Process whereby the immune system reacts against the body's own tissues. Autoimmunity may produce or be caused by AUTOIMMUNE DISEASES.
Disorders that are characterized by the production of antibodies that react with host tissues or immune effector cells that are autoreactive to endogenous peptides.
Antibodies that react with self-antigens (AUTOANTIGENS) of the organism that produced them.
Endogenous tissue constituents that have the ability to interact with AUTOANTIBODIES and cause an immune response.
A subtype of DIABETES MELLITUS that is characterized by INSULIN deficiency. It is manifested by the sudden onset of severe HYPERGLYCEMIA, rapid progression to DIABETIC KETOACIDOSIS, and DEATH unless treated with insulin. The disease may occur at any age, but is most common in childhood or adolescence.
Mercury chloride (HgCl2). A highly toxic compound that volatizes slightly at ordinary temperature and appreciably at 100 degrees C. It is corrosive to mucous membranes and used as a topical antiseptic and disinfectant.
A chronic, relapsing, inflammatory, and often febrile multisystemic disorder of connective tissue, characterized principally by involvement of the skin, joints, kidneys, and serosal membranes. It is of unknown etiology, but is thought to represent a failure of the regulatory mechanisms of the autoimmune system. The disease is marked by a wide range of system dysfunctions, an elevated erythrocyte sedimentation rate, and the formation of LE cells in the blood or bone marrow.
Lymphocytes responsible for cell-mediated immunity. Two types have been identified - cytotoxic (T-LYMPHOCYTES, CYTOTOXIC) and helper T-lymphocytes (T-LYMPHOCYTES, HELPER-INDUCER). They are formed when lymphocytes circulate through the THYMUS GLAND and differentiate to thymocytes. When exposed to an antigen, they divide rapidly and produce large numbers of new T cells sensitized to that antigen.
Autoantibodies directed against various nuclear antigens including DNA, RNA, histones, acidic nuclear proteins, or complexes of these molecular elements. Antinuclear antibodies are found in systemic autoimmune diseases including systemic lupus erythematosus, Sjogren's syndrome, scleroderma, polymyositis, and mixed connective tissue disease.
The normal lack of the ability to produce an immunological response to autologous (self) antigens. A breakdown of self tolerance leads to autoimmune diseases. The ability to recognize the difference between self and non-self is the prime function of the immune system.
CD4-positive T cells that inhibit immunopathology or autoimmune disease in vivo. They inhibit the immune response by influencing the activity of other cell types. Regulatory T-cells include naturally occurring CD4+CD25+ cells, IL-10 secreting Tr1 cells, and Th3 cells.
The specific failure of a normally responsive individual to make an immune response to a known antigen. It results from previous contact with the antigen by an immunologically immature individual (fetus or neonate) or by an adult exposed to extreme high-dose or low-dose antigen, or by exposure to radiation, antimetabolites, antilymphocytic serum, etc.
Inflammatory disease of the THYROID GLAND due to autoimmune responses leading to lymphocytic infiltration of the gland. It is characterized by the presence of circulating thyroid antigen-specific T-CELLS and thyroid AUTOANTIBODIES. The clinical signs can range from HYPOTHYROIDISM to THYROTOXICOSIS depending on the type of autoimmune thyroiditis.
A strain of non-obese diabetic mice developed in Japan that has been widely studied as a model for T-cell-dependent autoimmune insulin-dependent diabetes mellitus in which insulitis is a major histopathologic feature, and in which genetic susceptibility is strongly MHC-linked.
Morphologic alteration of small B LYMPHOCYTES or T LYMPHOCYTES in culture into large blast-like cells able to synthesize DNA and RNA and to divide mitotically. It is induced by INTERLEUKINS; MITOGENS such as PHYTOHEMAGGLUTININS, and by specific ANTIGENS. It may also occur in vivo as in GRAFT REJECTION.
Lymphoid cells concerned with humoral immunity. They are short-lived cells resembling bursa-derived lymphocytes of birds in their production of immunoglobulin upon appropriate stimulation.
A mouse substrain that is genetically predisposed to the development of systemic lupus erythematosus-like syndrome, which has been found to be clinically similar to the human disease. It has been determined that this mouse strain carries a mutation in the fas gene. Also, the MRL/lpr is a useful model to study behavioral and cognitive deficits found in autoimmune diseases and the efficacy of immunosuppressive agents.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
An experimental animal model for central nervous system demyelinating disease. Inoculation with a white matter emulsion combined with FREUND'S ADJUVANT, myelin basic protein, or purified central myelin triggers a T cell-mediated immune response directed towards central myelin. The pathologic features are similar to MULTIPLE SCLEROSIS, including perivascular and periventricular foci of inflammation and demyelination. Subpial demyelination underlying meningeal infiltrations also occurs, which is also a feature of ENCEPHALOMYELITIS, ACUTE DISSEMINATED. Passive immunization with T-cells from an afflicted animal to a normal animal also induces this condition. (From Immunol Res 1998;17(1-2):217-27; Raine CS, Textbook of Neuropathology, 2nd ed, p604-5)
Disorders caused by cellular or humoral immune responses primarily directed towards nervous system autoantigens. The immune response may be directed towards specific tissue components (e.g., myelin) and may be limited to the central nervous system (e.g., MULTIPLE SCLEROSIS) or the peripheral nervous system (e.g., GUILLAIN-BARRE SYNDROME).
A pyridoxal-phosphate protein that catalyzes the alpha-decarboxylation of L-glutamic acid to form gamma-aminobutyric acid and carbon dioxide. The enzyme is found in bacteria and in invertebrate and vertebrate nervous systems. It is the rate-limiting enzyme in determining GAMMA-AMINOBUTYRIC ACID levels in normal nervous tissues. The brain enzyme also acts on L-cysteate, L-cysteine sulfinate, and L-aspartate. EC 4.1.1.15.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
A critical subpopulation of T-lymphocytes involved in the induction of most immunological functions. The HIV virus has selective tropism for the T4 cell which expresses the CD4 phenotypic marker, a receptor for HIV. In fact, the key element in the profound immunosuppression seen in HIV infection is the depletion of this subset of T-lymphocytes.
Form of passive immunization where previously sensitized immunologic agents (cells or serum) are transferred to non-immune recipients. When transfer of cells is used as a therapy for the treatment of neoplasms, it is called adoptive immunotherapy (IMMUNOTHERAPY, ADOPTIVE).
A proinflammatory cytokine produced primarily by T-LYMPHOCYTES or their precursors. Several subtypes of interleukin-17 have been identified, each of which is a product of a unique gene.
Irregular microscopic structures consisting of cords of endocrine cells that are scattered throughout the PANCREAS among the exocrine acini. Each islet is surrounded by connective tissue fibers and penetrated by a network of capillaries. There are four major cell types. The most abundant beta cells (50-80%) secrete INSULIN. Alpha cells (5-20%) secrete GLUCAGON. PP cells (10-35%) secrete PANCREATIC POLYPEPTIDE. Delta cells (~5%) secrete SOMATOSTATIN.
The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.
Theoretical representations that simulate the behavior or activity of immune system, processes, or phenomena. They include the use of mathematical equations, computers, and other electrical equipment.
A subclass of winged helix DNA-binding proteins that share homology with their founding member fork head protein, Drosophila.
A classification of T-lymphocytes, especially into helper/inducer, suppressor/effector, and cytotoxic subsets, based on structurally or functionally different populations of cells.
Specialized cells of the hematopoietic system that have branch-like extensions. They are found throughout the lymphatic system, and in non-lymphoid tissues such as SKIN and the epithelia of the intestinal, respiratory, and reproductive tracts. They trap and process ANTIGENS, and present them to T-CELLS, thereby stimulating CELL-MEDIATED IMMUNITY. They are different from the non-hematopoietic FOLLICULAR DENDRITIC CELLS, which have a similar morphology and immune system function, but with respect to humoral immunity (ANTIBODY PRODUCTION).
Autoimmune diseases affecting multiple endocrine organs. Type I is characterized by childhood onset and chronic mucocutaneous candidiasis (CANDIDIASIS, CHRONIC MUCOCUTANEOUS), while type II exhibits any combination of adrenal insufficiency (ADDISON'S DISEASE), lymphocytic thyroiditis (THYROIDITIS, AUTOIMMUNE;), HYPOPARATHYROIDISM; and gonadal failure. In both types organ-specific ANTIBODIES against a variety of ENDOCRINE GLANDS have been detected. The type II syndrome differs from type I in that it is associated with HLA-A1 and B8 haplotypes, onset is usually in adulthood, and candidiasis is not present.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
An encapsulated lymphatic organ through which venous blood filters.
Antibodies specific to INSULIN.
A highly vascularized endocrine gland consisting of two lobes joined by a thin band of tissue with one lobe on each side of the TRACHEA. It secretes THYROID HORMONES from the follicular cells and CALCITONIN from the parafollicular cells thereby regulating METABOLISM and CALCIUM level in blood, respectively.
Subset of helper-effector T-lymphocytes which synthesize and secrete IL-17, IL-17F, and IL-22. These cytokines are involved in host defenses and tissue inflammation in autoimmune diseases.
A form of cutaneous tuberculosis. It is seen predominantly in women and typically involves the NASAL MUCOSA; BUCCAL MUCOSA; and conjunctival mucosa.
A tumor necrosis factor superfamily member that plays a role in the regulation of B-LYMPHOCYTE survival. It occurs as a membrane-bound protein that is cleaved to release an biologically active soluble form with specificity to TRANSMEMBRANE ACTIVATOR AND CAML INTERACTOR PROTEIN; B-CELL ACTIVATION FACTOR RECEPTOR; and B-CELL MATURATION ANTIGEN.
A single, unpaired primary lymphoid organ situated in the MEDIASTINUM, extending superiorly into the neck to the lower edge of the THYROID GLAND and inferiorly to the fourth costal cartilage. It is necessary for normal development of immunologic function early in life. By puberty, it begins to involute and much of the tissue is replaced by fat.
A subtype of non-receptor protein tyrosine phosphatases that is characterized by the presence of an N-terminal catalytic domain and a C-terminal PROLINE-rich domain. The phosphatase subtype is predominantly expressed in LYMPHOCYTES and plays a key role in the inhibition of downstream T-LYMPHOCYTE activation. Polymorphisms in the gene that encodes this phosphatase subtype are associated with a variety of AUTOIMMUNE DISEASES.
Subpopulation of CD4+ lymphocytes that cooperate with other lymphocytes (either T or B) to initiate a variety of immune functions. For example, helper-inducer T-cells cooperate with B-cells to produce antibodies to thymus-dependent antigens and with other subpopulations of T-cells to initiate a variety of cell-mediated immune functions.
Chronic autoimmune thyroiditis, characterized by the presence of high serum thyroid AUTOANTIBODIES; GOITER; and HYPOTHYROIDISM.
Molecules on the surface of T-lymphocytes that recognize and combine with antigens. The receptors are non-covalently associated with a complex of several polypeptides collectively called CD3 antigens (ANTIGENS, CD3). Recognition of foreign antigen and the major histocompatibility complex is accomplished by a single heterodimeric antigen-receptor structure, composed of either alpha-beta (RECEPTORS, ANTIGEN, T-CELL, ALPHA-BETA) or gamma-delta (RECEPTORS, ANTIGEN, T-CELL, GAMMA-DELTA) chains.
A disorder consisting of areas of macular depigmentation, commonly on extensor aspects of extremities, on the face or neck, and in skin folds. Age of onset is often in young adulthood and the condition tends to progress gradually with lesions enlarging and extending until a quiescent state is reached.
Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake.
The structure of one molecule that imitates or simulates the structure of a different molecule.
Non-antibody proteins secreted by inflammatory leukocytes and some non-leukocytic cells, that act as intercellular mediators. They differ from classical hormones in that they are produced by a number of tissue or cell types rather than by specialized glands. They generally act locally in a paracrine or autocrine rather than endocrine manner.
A classification of B-lymphocytes based on structurally or functionally different populations of cells.
An inhibitory T CELL receptor that is closely related to CD28 ANTIGEN. It has specificity for CD80 ANTIGEN and CD86 ANTIGEN and acts as a negative regulator of peripheral T cell function. CTLA-4 antigen is believed to play role in inducing PERIPHERAL TOLERANCE.
A hemeprotein that catalyzes the oxidation of the iodide radical to iodine with the subsequent iodination of many organic compounds, particularly proteins. EC 1.11.1.8.
Reduction in the number of lymphocytes.
An autoimmune disorder mainly affecting young adults and characterized by destruction of myelin in the central nervous system. Pathologic findings include multiple sharply demarcated areas of demyelination throughout the white matter of the central nervous system. Clinical manifestations include visual loss, extra-ocular movement disorders, paresthesias, loss of sensation, weakness, dysarthria, spasticity, ataxia, and bladder dysfunction. The usual pattern is one of recurrent attacks followed by partial recovery (see MULTIPLE SCLEROSIS, RELAPSING-REMITTING), but acute fulminating and chronic progressive forms (see MULTIPLE SCLEROSIS, CHRONIC PROGRESSIVE) also occur. (Adams et al., Principles of Neurology, 6th ed, p903)
Pathological processes involving the THYROID GLAND.
A group of the D-related HLA antigens found to differ from the DR antigens in genetic locus and therefore inheritance. These antigens are polymorphic glycoproteins comprising alpha and beta chains and are found on lymphoid and other cells, often associated with certain diseases.
A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.
Subset of helper-inducer T-lymphocytes which synthesize and secrete interleukin-2, gamma-interferon, and interleukin-12. Due to their ability to kill antigen-presenting cells and their lymphokine-mediated effector activity, Th1 cells are associated with vigorous delayed-type hypersensitivity reactions.
The major interferon produced by mitogenically or antigenically stimulated LYMPHOCYTES. It is structurally different from TYPE I INTERFERON and its major activity is immunoregulation. It has been implicated in the expression of CLASS II HISTOCOMPATIBILITY ANTIGENS in cells that do not normally produce them, leading to AUTOIMMUNE DISEASES.
B-cells that have a role in regulating the immune response including the production of CYTOKINES. This function is in addition to their traditional role in making antibodies.
A latent susceptibility to disease at the genetic level, which may be activated under certain conditions.
Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations, or by parent x offspring matings carried out with certain restrictions. All animals within an inbred strain trace back to a common ancestor in the twentieth generation.
Transmembrane proteins that form the beta subunits of the HLA-DQ antigens.
A critical subpopulation of regulatory T-lymphocytes involved in MHC Class I-restricted interactions. They include both cytotoxic T-lymphocytes (T-LYMPHOCYTES, CYTOTOXIC) and CD8+ suppressor T-lymphocytes.
Enlargement of the spleen.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
A fibrillar collagen found widely distributed as a minor component in tissues that contain COLLAGEN TYPE I and COLLAGEN TYPE III. It is a heterotrimeric molecule composed of alpha1(V), alpha2(V) and alpha3(V) subunits. Several forms of collagen type V exist depending upon the composition of the subunits that form the trimer.
Differentiation antigens residing on mammalian leukocytes. CD stands for cluster of differentiation, which refers to groups of monoclonal antibodies that show similar reactivity with certain subpopulations of antigens of a particular lineage or differentiation stage. The subpopulations of antigens are also known by the same CD designation.
A common form of hyperthyroidism with a diffuse hyperplastic GOITER. It is an autoimmune disorder that produces antibodies against the THYROID STIMULATING HORMONE RECEPTOR. These autoantibodies activate the TSH receptor, thereby stimulating the THYROID GLAND and hypersecretion of THYROID HORMONES. These autoantibodies can also affect the eyes (GRAVES OPHTHALMOPATHY) and the skin (Graves dermopathy).
The mechanism, in peripheral lymphoid organs (LYMPH NODES; SPLEEN; TONSILS; and mucosal-associated lymphoid tissue), that prevents mature lymphocytes from reacting to SELF-ANTIGENS. This is accomplished through a variety of means including CLONAL ANERGY and CLONAL DELETION.
The process by which antigen is presented to lymphocytes in a form they can recognize. This is performed by antigen presenting cells (APCs). Some antigens require processing before they can be recognized. Antigen processing consists of ingestion and partial digestion of the antigen by the APC, followed by presentation of fragments on the cell surface. (From Rosen et al., Dictionary of Immunology, 1989)
The capacity of a normal organism to remain unaffected by microorganisms and their toxins. It results from the presence of naturally occurring ANTI-INFECTIVE AGENTS, constitutional factors such as BODY TEMPERATURE and immediate acting immune cells such as NATURAL KILLER CELLS.
An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed.
Mouse strains constructed to possess identical genotypes except for a difference at a single gene locus.
Glomerulonephritis associated with autoimmune disease SYSTEMIC LUPUS ERYTHEMATOSUS. Lupus nephritis is histologically classified into 6 classes: class I - normal glomeruli, class II - pure mesangial alterations, class III - focal segmental glomerulonephritis, class IV - diffuse glomerulonephritis, class V - diffuse membranous glomerulonephritis, and class VI - advanced sclerosing glomerulonephritis (The World Health Organization classification 1982).
Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.
A chronic systemic disease, primarily of the joints, marked by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures. Etiology is unknown, but autoimmune mechanisms have been implicated.
Mice bearing mutant genes which are phenotypically expressed in the animals.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
A transmembrane protein present in the MYELIN SHEATH of the CENTRAL NERVOUS SYSTEM. It is one of the main autoantigens implicated in the pathogenesis of MULTIPLE SCLEROSIS.
A low affinity interleukin-2 receptor subunit that combines with the INTERLEUKIN-2 RECEPTOR BETA SUBUNIT and the INTERLEUKIN RECEPTOR COMMON GAMMA-CHAIN to form a high affinity receptor for INTERLEUKIN-2.
Chronic inflammatory and autoimmune disease in which the salivary and lacrimal glands undergo progressive destruction by lymphocytes and plasma cells resulting in decreased production of saliva and tears. The primary form, often called sicca syndrome, involves both KERATOCONJUNCTIVITIS SICCA and XEROSTOMIA. The secondary form includes, in addition, the presence of a connective tissue disease, usually rheumatoid arthritis.
An excess of GAMMA-GLOBULINS in the serum due to chronic infections or PARAPROTEINEMIAS.
Large, transmembrane, non-covalently linked glycoproteins (alpha and beta). Both chains can be polymorphic although there is more structural variation in the beta chains. The class II antigens in humans are called HLA-D ANTIGENS and are coded by a gene on chromosome 6. In mice, two genes named IA and IE on chromosome 17 code for the H-2 antigens. The antigens are found on B-lymphocytes, macrophages, epidermal cells, and sperm and are thought to mediate the competence of and cellular cooperation in the immune response. The term IA antigens used to refer only to the proteins encoded by the IA genes in the mouse, but is now used as a generic term for any class II histocompatibility antigen.
Manipulation of the host's immune system in treatment of disease. It includes both active and passive immunization as well as immunosuppressive therapy to prevent graft rejection.
A subclass of receptor-like protein tryosine phosphatases that contain an extracellular RDGS-adhesion recognition motif and a single cytosolic protein tyrosine phosphate domain.
An abundant cytosolic protein that plays a critical role in the structure of multilamellar myelin. Myelin basic protein binds to the cytosolic sides of myelin cell membranes and causes a tight adhesion between opposing cell membranes.
Alteration of the immune system or of an immune response by agents that activate or suppress its function. This can include IMMUNIZATION or administration of immunomodulatory drugs. Immunomodulation can also encompass non-therapeutic alteration of the immune system effected by endogenous or exogenous substances.
The body's defense mechanism against foreign organisms or substances and deviant native cells. It includes the humoral immune response and the cell-mediated response and consists of a complex of interrelated cellular, molecular, and genetic components.
Inflammation of part or all of the uvea, the middle (vascular) tunic of the eye, and commonly involving the other tunics (sclera and cornea, and the retina). (Dorland, 27th ed)
Deliberate stimulation of the host's immune response. ACTIVE IMMUNIZATION involves administration of ANTIGENS or IMMUNOLOGIC ADJUVANTS. PASSIVE IMMUNIZATION involves administration of IMMUNE SERA or LYMPHOCYTES or their extracts (e.g., transfer factor, immune RNA) or transplantation of immunocompetent cell producing tissue (thymus or bone marrow).
All of the processes involved in increasing CELL NUMBER including CELL DIVISION.
The production of ANTIBODIES by proliferating and differentiated B-LYMPHOCYTES under stimulation by ANTIGENS.
Surgical removal of the thymus gland. (Dorland, 28th ed)
Inflammatory diseases of the THYROID GLAND. Thyroiditis can be classified into acute (THYROIDITIS, SUPPURATIVE), subacute (granulomatous and lymphocytic), chronic fibrous (Riedel's), chronic lymphocytic (HASHIMOTO DISEASE), transient (POSTPARTUM THYROIDITIS), and other AUTOIMMUNE THYROIDITIS subtypes.
A heterogeneous group of immunocompetent cells that mediate the cellular immune response by processing and presenting antigens to the T-cells. Traditional antigen-presenting cells include MACROPHAGES; DENDRITIC CELLS; LANGERHANS CELLS; and B-LYMPHOCYTES. FOLLICULAR DENDRITIC CELLS are not traditional antigen-presenting cells, but because they hold antigen on their cell surface in the form of IMMUNE COMPLEXES for B-cell recognition they are considered so by some authors.
A condition characterized by persistent spasms (SPASM) involving multiple muscles, primarily in the lower limbs and trunk. The illness tends to occur in the fourth to sixth decade of life, presenting with intermittent spasms that become continuous. Minor sensory stimuli, such as noise and light touch, precipitate severe spasms. Spasms do not occur during sleep and only rarely involve cranial muscles. Respiration may become impaired in advanced cases. (Adams et al., Principles of Neurology, 6th ed, p1492; Neurology 1998 Jul;51(1):85-93)
ARTHRITIS that is induced in experimental animals. Immunological methods and infectious agents can be used to develop experimental arthritis models. These methods include injections of stimulators of the immune response, such as an adjuvant (ADJUVANTS, IMMUNOLOGIC) or COLLAGEN.
Sites on an antigen that interact with specific antibodies.
Subset of helper-inducer T-lymphocytes which synthesize and secrete the interleukins IL-4, IL-5, IL-6, and IL-10. These cytokines influence B-cell development and antibody production as well as augmenting humoral responses.
Invasion of the host organism by microorganisms that can cause pathological conditions or diseases.
Protection from an infectious disease agent that is mediated by B- and T- LYMPHOCYTES following exposure to specific antigen, and characterized by IMMUNOLOGIC MEMORY. It can result from either previous infection with that agent or vaccination (IMMUNITY, ACTIVE), or transfer of antibody or lymphocytes from an immune donor (IMMUNIZATION, PASSIVE).
Antibodies produced by a single clone of cells.
A strain of Rattus norvegicus which is a model for spontaneous insulin-dependent diabetes mellitus (DIABETES MELLITUS, INSULIN-DEPENDENT).
A class of immunoglobulin bearing mu chains (IMMUNOGLOBULIN MU-CHAINS). IgM can fix COMPLEMENT. The name comes from its high molecular weight and originally being called a macroglobulin.
Disorders characterized by proliferation of lymphoid tissue, general or unspecified.
Diseases of LYMPH; LYMPH NODES; or LYMPHATIC VESSELS.
Receptors present on activated T-LYMPHOCYTES and B-LYMPHOCYTES that are specific for INTERLEUKIN-2 and play an important role in LYMPHOCYTE ACTIVATION. They are heterotrimeric proteins consisting of the INTERLEUKIN-2 RECEPTOR ALPHA SUBUNIT, the INTERLEUKIN-2 RECEPTOR BETA SUBUNIT, and the INTERLEUKIN RECEPTOR COMMON GAMMA-CHAIN.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
A cytokine produced by a variety of cell types, including T-LYMPHOCYTES; MONOCYTES; DENDRITIC CELLS; and EPITHELIAL CELLS that exerts a variety of effects on immunoregulation and INFLAMMATION. Interleukin-10 combines with itself to form a homodimeric molecule that is the biologically active form of the protein.
Syndromes in which there is a deficiency or defect in the mechanisms of immunity, either cellular or humoral.
Substances that are recognized by the immune system and induce an immune reaction.
Functional inactivation of T- or B-lymphocytes rendering them incapable of eliciting an immune response to antigen. This occurs through different mechanisms in the two kinds of lymphocytes and can contribute to SELF TOLERANCE.
A soluble substance elaborated by antigen- or mitogen-stimulated T-LYMPHOCYTES which induces DNA synthesis in naive lymphocytes.
Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.
A heterodimeric cytokine that plays a role in innate and adaptive immune responses. Interleukin-23 is comprised of a unique 19 kDa subunit and 40 kDa subunit that is shared with INTERLEUKIN-12. It is produced by DENDRITIC CELLS; MACROPHAGES and a variety of other immune cells
Immunosuppression by reduction of circulating lymphocytes or by T-cell depletion of bone marrow. The former may be accomplished in vivo by thoracic duct drainage or administration of antilymphocyte serum. The latter is performed ex vivo on bone marrow before its transplantation.
A subclass of HLA-D antigens that consist of alpha and beta chains. The inheritance of HLA-DR antigens differs from that of the HLA-DQ ANTIGENS and HLA-DP ANTIGENS.
Antigens expressed primarily on the membranes of living cells during sequential stages of maturation and differentiation. As immunologic markers they have high organ and tissue specificity and are useful as probes in studies of normal cell development as well as neoplastic transformation.
The transference of pancreatic islets within an individual, between individuals of the same species, or between individuals of different species.
Deliberate breeding of two different individuals that results in offspring that carry part of the genetic material of each parent. The parent organisms must be genetically compatible and may be from different varieties or closely related species.
A medical specialty concerned with the hypersensitivity of the individual to foreign substances and protection from the resultant infection or disorder.
Removal, via CELL DEATH, of immature lymphocytes that interact with antigens during maturation. For T-lymphocytes this occurs in the thymus and ensures that mature T-lymphocytes are self tolerant. B-lymphocytes may also undergo clonal deletion.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Soluble factors which stimulate growth-related activities of leukocytes as well as other cell types. They enhance cell proliferation and differentiation, DNA synthesis, secretion of other biologically active molecules and responses to immune and inflammatory stimuli.
Manifestations of the immune response which are mediated by antigen-sensitized T-lymphocytes via lymphokines or direct cytotoxicity. This takes place in the absence of circulating antibody or where antibody plays a subordinate role.
IMMUNOGLOBULINS on the surface of B-LYMPHOCYTES. Their MESSENGER RNA contains an EXON with a membrane spanning sequence, producing immunoglobulins in the form of type I transmembrane proteins as opposed to secreted immunoglobulins (ANTIBODIES) which do not contain the membrane spanning segment.
Inflammatory processes of the muscular walls of the heart (MYOCARDIUM) which result in injury to the cardiac muscle cells (MYOCYTES, CARDIAC). Manifestations range from subclinical to sudden death (DEATH, SUDDEN). Myocarditis in association with cardiac dysfunction is classified as inflammatory CARDIOMYOPATHY usually caused by INFECTION, autoimmune diseases, or responses to toxic substances. Myocarditis is also a common cause of DILATED CARDIOMYOPATHY and other cardiomyopathies.
A constitution or condition of the body which makes the tissues react in special ways to certain extrinsic stimuli and thus tends to make the individual more than usually susceptible to certain diseases.
The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges.
A silver metallic element that exists as a liquid at room temperature. It has the atomic symbol Hg (from hydrargyrum, liquid silver), atomic number 80, and atomic weight 200.59. Mercury is used in many industrial applications and its salts have been employed therapeutically as purgatives, antisyphilitics, disinfectants, and astringents. It can be absorbed through the skin and mucous membranes which leads to MERCURY POISONING. Because of its toxicity, the clinical use of mercury and mercurials is diminishing.
Antigenic determinants recognized and bound by the T-cell receptor. Epitopes recognized by the T-cell receptor are often located in the inner, unexposed side of the antigen, and become accessible to the T-cell receptors after proteolytic processing of the antigen.
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
Acquired hemolytic anemia due to the presence of AUTOANTIBODIES which agglutinate or lyse the patient's own RED BLOOD CELLS.
The number of LYMPHOCYTES per unit volume of BLOOD.
T-cell receptors composed of CD3-associated alpha and beta polypeptide chains and expressed primarily in CD4+ or CD8+ T-cells. Unlike immunoglobulins, the alpha-beta T-cell receptors recognize antigens only when presented in association with major histocompatibility (MHC) molecules.
Multi-subunit proteins which function in IMMUNITY. They are produced by B LYMPHOCYTES from the IMMUNOGLOBULIN GENES. They are comprised of two heavy (IMMUNOGLOBULIN HEAVY CHAINS) and two light chains (IMMUNOGLOBULIN LIGHT CHAINS) with additional ancillary polypeptide chains depending on their isoforms. The variety of isoforms include monomeric or polymeric forms, and transmembrane forms (B-CELL ANTIGEN RECEPTORS) or secreted forms (ANTIBODIES). They are divided by the amino acid sequence of their heavy chains into five classes (IMMUNOGLOBULIN A; IMMUNOGLOBULIN D; IMMUNOGLOBULIN E; IMMUNOGLOBULIN G; IMMUNOGLOBULIN M) and various subclasses.
Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the ANTIGEN (or a very similar shape) that induced their synthesis in cells of the lymphoid series (especially PLASMA CELLS).
The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes IMMUNE COMPLEX DISEASES.
A type of pancreatic cell representing about 50-80% of the islet cells. Beta cells secrete INSULIN.
The processes whereby the internal environment of an organism tends to remain balanced and stable.
Inflammation of the renal glomeruli (KIDNEY GLOMERULUS) that can be classified by the type of glomerular injuries including antibody deposition, complement activation, cellular proliferation, and glomerulosclerosis. These structural and functional abnormalities usually lead to HEMATURIA; PROTEINURIA; HYPERTENSION; and RENAL INSUFFICIENCY.
They are oval or bean shaped bodies (1 - 30 mm in diameter) located along the lymphatic system.
A member of the tumor necrosis factor receptor superfamily that specifically binds B-CELL ACTIVATING FACTOR. It is found on B-LYMPHOCYTES and plays a role in maturation and survival of B-cells. Signaling by the activated receptor occurs through its association with TNF RECEPTOR-ASSOCIATED FACTORS.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
55-kDa antigens found on HELPER-INDUCER T-LYMPHOCYTES and on a variety of other immune cell types. CD4 antigens are members of the immunoglobulin supergene family and are implicated as associative recognition elements in MAJOR HISTOCOMPATIBILITY COMPLEX class II-restricted immune responses. On T-lymphocytes they define the helper/inducer subset. CD4 antigens also serve as INTERLEUKIN-15 receptors and bind to the HIV receptors, binding directly to the HIV ENVELOPE PROTEIN GP120.
Antibody-mediated immune response. Humoral immunity is brought about by ANTIBODY FORMATION, resulting from TH2 CELLS activating B-LYMPHOCYTES, followed by COMPLEMENT ACTIVATION.
Loss of scalp and body hair involving microscopically inflammatory patchy areas.
A tumor necrosis factor receptor subtype found in a variety of tissues and on activated LYMPHOCYTES. It has specificity for FAS LIGAND and plays a role in regulation of peripheral immune responses and APOPTOSIS. Multiple isoforms of the protein exist due to multiple ALTERNATIVE SPLICING. The activated receptor signals via a conserved death domain that associates with specific TNF RECEPTOR-ASSOCIATED FACTORS in the CYTOPLASM.
The property of antibodies which enables them to react with some ANTIGENIC DETERMINANTS and not with others. Specificity is dependent on chemical composition, physical forces, and molecular structure at the binding site.
The activated center of a lymphoid follicle in secondary lymphoid tissue where B-LYMPHOCYTES are stimulated by antigens and helper T cells (T-LYMPHOCYTES, HELPER-INDUCER) are stimulated to generate memory cells.
A costimulatory ligand expressed by ANTIGEN-PRESENTING CELLS that binds to CTLA-4 ANTIGEN with high specificity and to CD28 ANTIGEN with low specificity. The interaction of CD80 with CD28 ANTIGEN provides a costimulatory signal to T-LYMPHOCYTES, while its interaction with CTLA-4 ANTIGEN may play a role in inducing PERIPHERAL TOLERANCE.
The altered state of immunologic responsiveness resulting from initial contact with antigen, which enables the individual to produce antibodies more rapidly and in greater quantity in response to secondary antigenic stimulus.
The genetic region which contains the loci of genes which determine the structure of the serologically defined (SD) and lymphocyte-defined (LD) TRANSPLANTATION ANTIGENS, genes which control the structure of the IMMUNE RESPONSE-ASSOCIATED ANTIGENS, HUMAN; the IMMUNE RESPONSE GENES which control the ability of an animal to respond immunologically to antigenic stimuli, and genes which determine the structure and/or level of the first four components of complement.
Group of chronic blistering diseases characterized histologically by ACANTHOLYSIS and blister formation within the EPIDERMIS.
Conditions characterized by loss or dysfunction of myelin (see MYELIN SHEATH) in the brain, spinal cord, or optic nerves secondary to autoimmune mediated processes. This may take the form of a humoral or cellular immune response directed toward myelin or OLIGODENDROGLIA associated autoantigens.
Process of classifying cells of the immune system based on structural and functional differences. The process is commonly used to analyze and sort T-lymphocytes into subsets based on CD antigens by the technique of flow cytometry.
A general term for diseases produced by viruses.
Glycoproteins found on the membrane or surface of cells.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
Antibodies found in adult RHEUMATOID ARTHRITIS patients that are directed against GAMMA-CHAIN IMMUNOGLOBULINS.
A chronic multi-system disorder of CONNECTIVE TISSUE. It is characterized by SCLEROSIS in the SKIN, the LUNGS, the HEART, the GASTROINTESTINAL TRACT, the KIDNEYS, and the MUSCULOSKELETAL SYSTEM. Other important features include diseased small BLOOD VESSELS and AUTOANTIBODIES. The disorder is named for its most prominent feature (hard skin), and classified into subsets by the extent of skin thickening: LIMITED SCLERODERMA and DIFFUSE SCLERODERMA.
A membrane glycoprotein and differentiation antigen expressed on the surface of T-cells that binds to CD40 ANTIGENS on B-LYMPHOCYTES and induces their proliferation. Mutation of the gene for CD40 ligand is a cause of HYPER-IGM IMMUNODEFICIENCY SYNDROME, TYPE 1.
An induced state of non-reactivity to grafted tissue from a donor organism that would ordinarily trigger a cell-mediated or humoral immune response.
A soluble factor produced by activated T-LYMPHOCYTES that induces the expression of MHC CLASS II GENES and FC RECEPTORS on B-LYMPHOCYTES and causes their proliferation and differentiation. It also acts on T-lymphocytes, MAST CELLS, and several other hematopoietic lineage cells.
White blood cells formed in the body's lymphoid tissue. The nucleus is round or ovoid with coarse, irregularly clumped chromatin while the cytoplasm is typically pale blue with azurophilic (if any) granules. Most lymphocytes can be classified as either T or B (with subpopulations of each), or NATURAL KILLER CELLS.

Fine specificity of the autoimmune response to the Ro/SSA and La/SSB ribonucleoproteins. (1/3192)

The fine specificity of the Ro and La proteins has been studied by several techniques. In general, there is agreement in a qualitative sense that autoantibodies bind multiple epitopes. For some specific antibody binding, different studies agree quantitatively, for instance, the binding of the carboxyl terminus of 60-kd Ro as described by 2 studies using different techniques and the presence of an epitope within the leucine zipper of 52-kd Ro. In addition, there is general agreement about the location of a prominent epitope at the RRM motif region of the La molecule. On the other hand, the many specific epitope regions of the molecules differ among these studies. These discrepancies are likely the result of using different techniques, sera, and peptide constructs as well as a result of inherent advantages and disadvantages in the individual approaches. Several theories concerning the origin of not only the antibodies, but also the diseases themselves, have been generated from studies of the fine specificity of antibody binding. These include a theory of a primordial foreign antigen for anti-Ro autoimmunity, molecular mimicry with regard to La and CCHB, as well as the association of anti-Ro with HLA. These remain unproven, but are of continuing interest. An explanation for the association of anti-60-kd Ro and anti-52-kd Ro in the sera of patients has sprung from evaluating antibody binding. Data demonstrating multiple epitopes are part of a large body of evidence that strongly suggests an antigen-driven immune response. This means that the autoantigens are directly implicated in initiating and sustaining autoimmunity in their associated diseases. A number of studies have investigated the possibility of differences in the immune response to these antigens in SS and SLE sera. While several differences have been reported, none have been reproduced in a second cohort of patients. Furthermore, none of the reported differences may be sufficiently robust for clinical purposes, such as distinguishing between SS with systemic features and mild SLE, although some might be promising. For instance, in at least 3 groups of SLE patients, no binding of residues spanning amino acids 21-41 of 60-kd Ro has been found. Meanwhile, 1 of those studies found that 41% of sera from patients with primary SS bound the 60-kd Ro peptide 21-41. Perhaps future studies will elaborate a clinical role of such a difference among SS and SLE patients. Study of the epitopes of these autoantigens has, in part, led to a new animal model of anti-Ro and anti-La. Non-autoimmune-prone animals are immunized with proteins or peptides that make up the Ro/La RNP. Such animals develop an autoimmune response to the entire particle, not just the immunogen. This response has been hypothesized to arise from autoreactive B cells. In another, older animal model of disease, the MRL-lpr/lpr mouse, B cells have recently been shown to be required for the generation of abnormal, autoreactive T cells. Thus, there are now powerful data indicating that B cells that produce autoantibodies are directly involved in the pathogenesis of disease above and beyond the formation of immune complexes. Given that the autoreactive B cell is potentially critical to the underlying pathogenesis of disease, then studying these cells will be crucial to further understanding the origin of diseases associated with Ro and La autoimmunity. Hopefully, an increased understanding will eventually lead to improved treatment of patients. Progress in the area of treatment will almost surely be incremental, and studies of the fine specificity of autoantibody binding will be a part of the body of basic knowledge contributing to ultimate advancement. In the future, the animal models will need to be examined with regard to immunology and immunochemistry as well as genetics. The development of these autoantibodies has not been studied extensively because upon presentation to medical care, virtually all patients have a full-  (+info)

Development and function of autospecific dual TCR+ T lymphocytes. (2/3192)

Recent studies have challenged the long held concept that each T lymphocyte expresses on its surface only a single, unique alphabetaTCR. Dual TCR+ T cells have been recognized, however, their origin and potential to escape screening for self-reactivity remain obscure. We now report the thymic generation of dual alphabetaTCR+ T cells in the H-2Db/H-Y-specific TCR transgenic (Tg) mouse. Dual TCR+ thymocytes were positively selected less efficiently than single TCR+ thymocytes, although a subset attained maturity. Importantly, when TCR Tg mice were bred onto a negatively selecting background, auto-specific cells survived central deletion and matured as CD4+ dual TCR+ cells. These cells were autoreactive when CD8 expression was restored. The existence of autospecific, dual TCR+ T cells may have implications for the maintenance of self tolerance.  (+info)

Induction of autoimmunity by multivalent immunodominant and subdominant T cell determinants of La (SS-B). (3/3192)

We investigated the consequences of altering the form and valence of defined autodeterminants on the initiation and spreading of experimentally induced La/Ro autoimmunity. Anti-La and Ro (SS-A) Ab responses were monitored following immunization of healthy mice with defined immunodominant and subdominant T cell determinants of the La (SS-B) autoantigen synthesized as either monomeric or multiple antigenic (MAP) peptides. Abs to mouse La (mLa) developed faster and were of higher titer in mice immunized with the subdominant mLa25-44 MAP compared with mice immunized with the 25-44 monomer. Rapid intermolecular spreading of the autoimmune response to 60-kDa Ro was observed in AKR/J mice immunized with mLa25-44 MAP, but not in mice immunized repeatedly with monomeric peptide. A/J mice immunized and boosted with the known tolerogenic mLa287-301 determinant delivered as monomeric peptide failed to develop Abs to either intact mLa or mLa287-301 peptide. However, immunization with the multivalent mLa287-301 peptide led to the rapid production of high titer mLa autoantibodies associated with a proliferative T cell response to the mLa287-301 peptide. The data suggested that the enhanced immunogenicity of MAPs was not due to augmented Ag presentation or T cell stimulation. However, MAP-, but not monomer peptide-, containing immune complexes were potent substrates for Ab-dependent fixation of complement. These results demonstrate that the form of Ag responsible for inducing autoimmunity can profoundly influence the nature and magnitude of the immune response. Thus, molecular mimicry of tolerogenic and nontolerogenic self determinants might trigger autoimmunity under conditions of altered valence.  (+info)

Clinical, biochemical and molecular genetic features of Leber's hereditary optic neuropathy. (4/3192)

Leber's hereditary optic neuropathy (LHON) has traditionally been considered a disease causing severe and permanent visual loss in young adult males. In nearly all families with LHON it is associated with one of three pathogenic mitochondrial DNA (mtDNA) mutations, at bp 11778, 3460 or 14484. The availability of mtDNA confirmation of a diagnosis of LHON has demonstrated that LHON occurs with a wider range of age at onset and more commonly in females than previously recognised. In addition, analysis of patients grouped according to mtDNA mutation has demonstrated differences both in the clinical features of visual failure and in recurrence risks to relatives associated with each of the pathogenic mtDNA mutations. Whilst pathogenic mtDNA mutations are required for the development of LHON, other factors must be reponsible for the variable penetrance and male predominance of this condition. Available data on a number of hypotheses including the role of an additional X-linked visual loss susceptibility locus, impaired mitochondrial respiratory chain activity, mtDNA heteroplasmy, environmental factors and autoimmunity are discussed. Subacute visual failure is seen in association with all three pathogenic LHON mutations. However, the clinical and experimental data reviewed suggest differences in the phenotype associated with each of the three mutations which may reflect variation in the disease mechanisms resulting in this common end-point.  (+info)

Vaccination with a recombinant vaccinia virus encoding a "self" antigen induces autoimmune vitiligo and tumor cell destruction in mice: requirement for CD4(+) T lymphocytes. (5/3192)

Many human and mouse tumor antigens are normal, nonmutated tissue differentiation antigens. Consequently, immunization with these "self" antigens could induce autoimmunity. When we tried to induce immune responses to five mouse melanocyte differentiation antigens, gp100, MART-1, tyrosinase, and tyrosinase-related proteins (TRP) 1 and TRP-2, we observed striking depigmentation and melanocyte destruction only in the skin of mice inoculated with a vaccinia virus encoding mouse TRP-1. These mice rejected a lethal challenge of B16 melanoma, indicating the immune response against TRP-1 could destroy both normal and malignant melanocytes. Cytotoxic T lymphocytes specific for TRP-1 could not be detected in depigmented mice, but high titers of IgG anti-TRP-1 antibodies were present. Experiments with knockout mice revealed an absolute dependence on major histocompatibility complex class II, but not major histocompatibility complex class I, for the induction of both vitiligo and tumor protection. Together, these results suggest that the deliberate induction of self-reactivity using a recombinant viral vector can lead to tumor destruction, and that in this model, CD4(+) T lymphocytes are an integral part of this process. Vaccine strategies targeting tissue differentiation antigens may be valuable in cancers arising from nonessential cells and organs such as melanocytes, prostate, testis, breast, and ovary.  (+info)

Autoimmunity resulting from cytokine treatment predicts long-term survival in patients with metastatic renal cell cancer. (6/3192)

PURPOSE: In patients undergoing cytokine therapy, systemically applied interleukin-2 (IL-2) and/or interferon-alpha (IFN-alpha) have been reported to induce thyroid dysfunction as well as thyroid autoantibodies. We analyzed the correlation of thyroid autoimmunity with HLA phenotype, various other autoimmune parameters, and patient survival. PATIENTS AND METHODS: For this purpose, antithyroglobulin autoantibodies, antimicrosomal thyroid autoantibodies, thyroglobulin receptor autoantibodies, thyroid dysfunction, and multiple clinical parameters were determined in 329 unselected patients with metastatic renal cell cancer before and after systemic IL-2 and IFN-alpha2 therapy. For statistical analysis, we used both univariate and multivariate Cox proportional hazards models and the two-tailed Fisher's exact test. RESULTS: Antithyroglobulin autoantibodies and antimicrosomal thyroid autoantibodies were detected in 60 patients (18%); positive autoantibody titers of various other autoimmune parameters were statistically unrelated. The presence of thyroid autoantibodies was correlated with prolonged survival (P<.0001). There was a statistically significant difference in frequencies of HLA-Cw7 expression between thyroid autoantibody-positive and -negative patients (P< or =.05), and the Cw7 expression was associated with prolonged overall survival (P = .009). CONCLUSION: The evaluation of thyroid autoantibodies during cytokine therapy could be a useful prognostic marker for patients with renal cell carcinoma who benefit from cytokine treatment. IL-2- and IFN-alpha2-induced tumor control and prolonged survival may require breaking of immunologic tolerance against self-antigens.  (+info)

Evidence of cell-mediated cardiac myocyte injury involved in the heart failure of a patient with progressive systemic sclerosis. (7/3192)

A 54-year-old woman with progressive systemic sclerosis (PSS) was admitted to hospital because of dyspnea and chest pain. Echocardiogram revealed diffuse hypokinesis of the left ventricle (ejection fraction 24%). Methylprednisolone, heparin, and diuretics were administered, without benefit. Anemia, thrombocytopenia, and renal dysfunction rapidly progressed, and she died of heart failure on the 14th hospital day. Immunohistochemical study of the myocardial tissue showed mild to moderate cell infiltration, mainly consisting of natural killer (NK) cells, macrophages, cytotoxic T lymphocytes (CTLs), and T helper cells. Perforin, a cytolytic factor, was expressed in the infiltrating CTLs and NK cells, indicating that these cells were activated killer cells. Furthermore, human leukocyte antigen classes I and II, intercellular adhesion molecule-1, as well as costimulatory molecules B7-1, B7-2, and CD40, all of which are known not to be expressed in cardiac myocytes under normal conditions, were moderately to strongly expressed in cardiac myocytes. There was no detectable level of enterovirus genomes in the polymerase chain reaction products from the myocardial tissue of this patient. These findings strongly suggest that the infiltrating killer cells recognized cardiac myocytes as target cells and directly damaged them by releasing perforin. Enhanced expression of these antigens may have played an important role in the activation and cytotoxicity of the infiltrating killer cells. Absence of enterovirus genomes in the myocardial tissue may suggest that this autoimmune process is primarily induced by PSS.  (+info)

Clinical presentation and early course of type 1 diabetes in patients with and without thyroid autoimmunity. (8/3192)

OBJECTIVE: To evaluate the prevalence of thyroid autoimmunity (TAI) in patients with recent-onset type 1 diabetes and to determine the influence of TAI on the clinical presentation and evolution of type 1 diabetes. RESEARCH DESIGN AND METHODS: We studied 111 newly diagnosed type 1 diabetes patients > 13 years old. The diagnosis of TAI was based on medical history and measurement of thyroid peroxidase (microsomal) antibodies (TPOAs). Clinical presentation of diabetes, beta-cell autoimmune markers (GADAs and 1A2As), and evolution of insulin-secretory reserves and metabolic control during the first 2 years of follow-up were analyzed. Differences between groups were evaluated by Student's t test or the chi 2 test. The influence of TAI on follow-up data was evaluated by multiple logistic regression analysis. RESULTS: TAI was present in 31 patients (14 TPOA+ patients with normal thyroid function, 12 TPOA+ patients with thyroid dysfunction, and 5 patients with previously diagnosed TAI). TAI was more prevalent in women than in men (43.7 vs. 15.9%, P = 0.001). beta-Cell autoimmunity was more prevalent in patients with TAI than in those without TAI (93.5 vs. 76.3%, P = 0.03). The evolution of insulin requirements, metabolic control, and insulin-secretory reserves was comparable in the two groups. CONCLUSIONS: TAI is present in many type 1 diabetes patients at the time of diagnosis and is associated with a high prevalence of thyroid dysfunction. The clinical presentation of diabetes and the evolution of metabolic control and insulin-secretory reserves are not influenced by the presence of TAI. Patients with type 1 diabetes should be screened for TAI at diagnosis.  (+info)

TY - JOUR. T1 - Definition of human autoimmunity - autoantibodies versus autoimmune disease. AU - Lleo, Ana. AU - Invernizzi, Pietro. AU - Gao, Bin. AU - Podda, Mauro. AU - Gershwin, M. Eric. PY - 2010/3. Y1 - 2010/3. N2 - The critical function of the immune system is to discriminate self from non-self. Tolerance against self-antigens is a highly regulated process and, in order to maintain it, the immune system must be able to distinguish self-reactive lymphocytes as they develop. The presence of autoantibodies is the consequence of breakdown of tolerance and, although they are an important serological feature of autoimmune diseases, their presence is not exclusive of these conditions. Antibodies against self-antigens are also found in cancer, during massive tissue damage and even in healthy subjects. Natural autoantibodies provide immediate protection against infection and also prevent inflammation by facilitating the clearance of oxidized lipids, oxidized proteins, and apoptotic cells; their ...
Although high expression of most B7 family members is largely restricted to immune cells, especially APCs, we were not able to detect protein expression of B7x in any cell type of hematopoietic origin. This strongly suggested that B7x does not play a role in regulating T cell priming in the lymphoid organs. However, histological staining of pancreatic sections demonstrated constitutive expression of B7x in the islets of Langerhans, indicating that this inhibitory molecule may have a role in maintaining peripheral tolerance to islet-reactive T cells. It has already been shown that PD-L1, another member of the B7 family, plays an important role in preventing diabetes by inhibiting islet-reactive T cells (Ansari et al., 2003). Although PD-L1 has been reported to be expressed at very low levels (Liang et al., 2003) or absent (Ansari et al., 2003) in naive pancreata, its expression is up-regulated in an age-dependent manner in NOD mice. Using bone marrow chimeras, it was shown that PD-L1 expression ...
Understanding the mode of action of genes influencing the development of type 1 diabetes requires knowledge as to whether genes influence the development of islet autoimmunity and/or progression from autoimmunity to diabetes. Here we have examined association in a cohort of genetically at-risk children who were followed from birth for both development of islet autoantibodies and diabetes. An association of the IFIH1 gene with diabetes development in this cohort allowed us to determine at what stage the gene is likely to influence diabetes development. Unlike HLA class II genes, which strongly influence the risk for developing islet autoantibodies (5-7), association of the IFIH1 gene was restricted to the progression to diabetes after development of islet autoimmunity. In view of the involvement of the IFIH1 gene in responses to virus infection (16,17), the findings are consistent with a role of infection in determining the progression to diabetes after islet autoimmunity has been ...
TY - JOUR. T1 - Helper T cells in antibody-mediated, organ-specific autoimmunity. AU - Elson, C J AU - Barker, R N PY - 2000. Y1 - 2000. N2 - The production of pathogenic autoantibodies in organ-specific autoimmune diseases is largely T cell dependent. For many of these diseases, the precise specificities and cytokine profiles of the T cells that respond to the corresponding autoantigens have now been identified. This knowledge has been exploited to treat some models of antibody-mediated autoimmunity using peptides corresponding to the dominant helper epitopes, giving impetus to the development of a similar approach in the equivalent human diseases.. AB - The production of pathogenic autoantibodies in organ-specific autoimmune diseases is largely T cell dependent. For many of these diseases, the precise specificities and cytokine profiles of the T cells that respond to the corresponding autoantigens have now been identified. This knowledge has been exploited to treat some models of ...
A better understanding of the molecules involved in immune responses has identified many potential targets for the treatment of autoimmune diseases. But although successful therapies have been found for immune disorders in animal studies, few have passed the much harder test of treating human diseases. So far, non-antigen-specific approaches, such as the blocking of tumour-necrosis factor, are achieving some success but the same is not true for antigen-specific approaches. Future therapies will probably include both non-antigen-specific strategies that target cytokines (cell-cell signalling molecules) or block the molecules that stimulate immune responses, and antigen-specific therapies that induce tolerance to self antigens.
TY - JOUR. T1 - Increased serum IgM, immunodeficiency, and autoimmunity. T2 - A clinical series. AU - Picchianti Diamanti, Andrea. AU - Rosado, M. Manuela. AU - Scarsella, Marco. AU - Ceccarelli, Sara. AU - Laganà, Bruno. AU - DAmelio, Raffaele. AU - Carsetti, Rita. PY - 2015/12/1. Y1 - 2015/12/1. N2 - Background: Primary immunodeficiencies (PIDs) are generally characterized by recurrent infections; however they may be complicated by other clinical disorders such as allergy, autoimmunity, and lymphoproliferation. In particular, autoimmunity may be the first manifestation of the disease in patients with low serum immunoglobulins (Ig) levels. Here we describe a group of patients that share features of immunodeficiency and autoimmunity. Materials and Methods: All patients went through a complete T and B cell subset characterization and a B cell function analysis in the peripheral blood by flow-cytometry. B cell proliferation and plasma cell differentiation was measured, in vitro, after CpG ...
Systemic autoimmunity is thought to result from a mix of genetics, environmental factors and stochastic events [6]. Given the multitude of susceptibility genes, symptoms and immunological abnormalities, it is clear that numerous pathogenic pathways contribute to systemic autoimmune disease [5, 11, 12]. A major thrust of systemic autoimmunity research has centered on elucidation of abnormalities in the adaptive immune response [13, 14]. However more recent research has identified the innate immune response as a major player in the initiation and expansion of systemic autoimmune pathology [4, 5, 9, 15, 16].. The current paradigm for the disease process of idiopathic systemic lupus-like autoimmunity argues for a central role of type I IFN [15, 17, 18]. This is based on the early observation of increased expression of IFN-α inducible genes (or IFN signature) in the peripheral blood cells of patients with SLE [17]. The type I IFN signature is found in 60% to 70% of patients with SLE, ...
Autoimmunity causing insulin-dependent diabetes mellitus (IDDM) begins in early childhood due to interactions between genes and unknown environmental factors that may be identified through follow-up of a large cohort of genetically susceptible children. Such a cohort has been established using a sim …
Curing type 1 diabetes by islet transplantation requires overcoming both allorejection and recurrent autoimmunity. This has been achieved with systemic immunosuppression, but tolerance induction would be preferable. Most islet allotransplant tolerance induction protocols have been tested in nonobese diabetic (NOD) mice, and most have failed. Failure has been attributed to the underlying autoimmunity, assuming that autoimmunity and resistance to transplantation tolerance have a common basis. Out of concern that NOD biology could be misleading in this regard, we tested the hypothesis that autoimmunity and resistance to transplantation tolerance in NOD mice are distinct phenotypes. Unexpectedly, we observed that (NOD x C57BL/6)F(1) mice, which have no diabetes, nonetheless resist prolongation of skin allografts by costimulation blockade. Further analyses revealed that the F(1) mice shared the dendritic cell maturation defects and abnormal CD4(+) T cell responses of the NOD but had lost its defects in
Highlights: - Antibiotics being explored for the treatment of cystic fibrosis and muscular dystrophy have the potential to trigger autoimmune disease - . He identified 17 peptides that hadnt been characterized before in cells treated with gentamicin and showed that the peptides were presentable to the immune system. - So even as gentamicin fights the…
Lindop, R., et al. Long-term Ro60 humoral autoimmunity in primary Sjögrens syndrome is maintained by rapid clonal turnover. Clinical Immunology. 0, 148(1). 01/07/2013.. ...
Some people seem to be under the belief that autoimmune conditions such as type-1 diabetes develop as a result of bad genes. This idea has little evolutionary support…. Theres no doubt that genetics do play a role in the etiology of autoimmunity; however, in most cases, its unlikely to be the primary factor involved. This statement is supported by the fact that the prevalence of autoimmune disease has increased markedly over the past centuries, despite the fact that our genes have changed very little over the same time period. Moreover, its supported by the finding that autoimmune diseases are very rare among hunter-gatherers and other traditional groups of people who live in environments that bear resemblance to the Paleolithic environments in which more than 99% of the evolutionary history of our genus Homo took place (1, 2, 3).. When we think about it, it isnt surprising that foragers rarely develop autoimmunity, given that a persons ability to survive and reproduce in a natural ...
They found that ANA (biomarker for autoimmunity) prevalence for 1988-1991 was 11.0%, while for 1999-2004 it was 11.5%, and for 2011-2012 it was 15.9%. These percentages corresponded to 22, 27, and 41 million affected individuals, respectively. ...
Recent evidences suggest that human gut microbiota with major component as bacteria can induce immunity. It is also known that gut lining depletes with ageing and that there is increased risk of autoimmune and inflammatory disorders with ageing. It is therefore likely that both may be correlated as depletion of gut lining exposes the gut bacterial antigens to host immune mechanisms, which may induce immunity to certain bacterial proteins, but at the same time such immunity may also be auto-immunogenic to host. This autoimmunity may make a protein molecule nonfunctional and thereby may be involved in late onset metabolic, autoimmune and inflammatory disorders such as, Diabetes, Rheumatoid Arthritis, Hyperlipidemias and Cancer. In this in-silico study we found a large number of peptides identical between human and gut bacteria which were binding to HLA-II alleles, and hence, likely to be auto-immunogenic. Further we observed that such autoimmune candidates were enriched in bacterial species belonging to
The best evidence to date shows a significant association between thyroid autoimmunity and depression & anxiety. But what does this mean and what should you do?
The exact role of graft tissue specific antigens in transplant rejection is unknown. Recently, we have detected CD4+ T cell- and B cell-mediated autoimmunity to...
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Overall, grade 3 or higher IRAEs developed in 10 of 23 patients following combination therapy, in 1 of 8 patients following anti-CTLA4 therapy, and in 1 of 8 patients following anti-PD1 therapy. The finding that CCB leads to higher rates of IRAEs as well as significant and distinct changes in B cells, including a decline in circulating B cells as well as an increase in CD21lo B cells and plasmablasts, led us to evaluate the correlation between these changes and the development of autoimmunity. Interestingly, the severity of an early decline in B cell numbers after therapy directly correlated with the time to onset of toxicity (Figure 3B; P = 0.007) as well as the grade of maximal toxicity (Figure 3C). The ability to identify patients at increased risk for developing autoimmunity is critical for the application of CCB. We developed a parameter for B cell changes following combination therapy by integrating the decline in B cell numbers (fold change after therapy, ≤70% of baseline) with a 2-fold ...
Overall, grade 3 or higher IRAEs developed in 10 of 23 patients following combination therapy, in 1 of 8 patients following anti-CTLA4 therapy, and in 1 of 8 patients following anti-PD1 therapy. The finding that CCB leads to higher rates of IRAEs as well as significant and distinct changes in B cells, including a decline in circulating B cells as well as an increase in CD21lo B cells and plasmablasts, led us to evaluate the correlation between these changes and the development of autoimmunity. Interestingly, the severity of an early decline in B cell numbers after therapy directly correlated with the time to onset of toxicity (Figure 3B; P = 0.007) as well as the grade of maximal toxicity (Figure 3C). The ability to identify patients at increased risk for developing autoimmunity is critical for the application of CCB. We developed a parameter for B cell changes following combination therapy by integrating the decline in B cell numbers (fold change after therapy, ≤70% of baseline) with a 2-fold ...
Overall, grade 3 or higher IRAEs developed in 10 of 23 patients following combination therapy, in 1 of 8 patients following anti-CTLA4 therapy, and in 1 of 8 patients following anti-PD1 therapy. The finding that CCB leads to higher rates of IRAEs as well as significant and distinct changes in B cells, including a decline in circulating B cells as well as an increase in CD21lo B cells and plasmablasts, led us to evaluate the correlation between these changes and the development of autoimmunity. Interestingly, the severity of an early decline in B cell numbers after therapy directly correlated with the time to onset of toxicity (Figure 3B; P = 0.007) as well as the grade of maximal toxicity (Figure 3C). The ability to identify patients at increased risk for developing autoimmunity is critical for the application of CCB. We developed a parameter for B cell changes following combination therapy by integrating the decline in B cell numbers (fold change after therapy, ≤70% of baseline) with a 2-fold ...
Autoimmunity Highlights acts as the bridge between the clinic, the laboratory and specialists involved in the complex world of autoimmunity diagnosis, ...
Autoimmunity Reviews will publish up-to-date, structured reviews on diverse topics in autoimmunity, written by first-class experts in the field. The...
Autoimmune diseases occur when the immune system attacks and destroys the organs and tissues of its own host. Autoimmunity is the third most common type of disease in the United States. Because there is no cure for autoimmunity, it is extremely important to study the mechanisms that trigger these diseases. Most autoimmune diseases predominantly affect females, indicating a strong sex bias. Various factors, including sex hormones, the presence or absence of a second X chromosome, and sex-specific gut microbiota can influence gene expression in a sex-specific way. These changes in gene expression may, in turn, lead to susceptibility or protection from autoimmunity, creating a sex bias for autoimmune diseases. In this Review we discuss recent findings in the field of sex-dependent regulation of gene expression and autoimmunity.. ...
Increasing evidence suggests that islet autoimmunity also targets neoepitopes expressed by the target cells, which may not be available for negative thymic selection. Differential expression of IA-2 and IGRP mRNAs in thymus and pancreas (157, 158) may promote autoimmunity, as the immune system may not be tolerant to alternatively spliced variants expressed in pancreas but not thymus (159). Many autoantigens in autoimmune disease are post-translationally modified (PTM) (160). Inflammation and stress are likely factors in the generation of PTM antigens, which derive from both normal and abnormal processes in cells. Predisposing HLA types are critical for the presentation of these epitopes to T cells (161, 162). Below, the major neoepitope classes associated with T1D are described.. Neoepitopes generated by PTM. A PTM epitope exists in the insulin A chain (A1-A13): T cell recognition requires oxidized cysteine residues at A6 and A7, with the formation of a vicinal disulfide bond between them (60). ...
Increasing evidence suggests that islet autoimmunity also targets neoepitopes expressed by the target cells, which may not be available for negative thymic selection. Differential expression of IA-2 and IGRP mRNAs in thymus and pancreas (157, 158) may promote autoimmunity, as the immune system may not be tolerant to alternatively spliced variants expressed in pancreas but not thymus (159). Many autoantigens in autoimmune disease are post-translationally modified (PTM) (160). Inflammation and stress are likely factors in the generation of PTM antigens, which derive from both normal and abnormal processes in cells. Predisposing HLA types are critical for the presentation of these epitopes to T cells (161, 162). Below, the major neoepitope classes associated with T1D are described.. Neoepitopes generated by PTM. A PTM epitope exists in the insulin A chain (A1-A13): T cell recognition requires oxidized cysteine residues at A6 and A7, with the formation of a vicinal disulfide bond between them (60). ...
Increasing evidence suggests that islet autoimmunity also targets neoepitopes expressed by the target cells, which may not be available for negative thymic selection. Differential expression of IA-2 and IGRP mRNAs in thymus and pancreas (157, 158) may promote autoimmunity, as the immune system may not be tolerant to alternatively spliced variants expressed in pancreas but not thymus (159). Many autoantigens in autoimmune disease are post-translationally modified (PTM) (160). Inflammation and stress are likely factors in the generation of PTM antigens, which derive from both normal and abnormal processes in cells. Predisposing HLA types are critical for the presentation of these epitopes to T cells (161, 162). Below, the major neoepitope classes associated with T1D are described.. Neoepitopes generated by PTM. A PTM epitope exists in the insulin A chain (A1-A13): T cell recognition requires oxidized cysteine residues at A6 and A7, with the formation of a vicinal disulfide bond between them (60). ...
Increasing evidence suggests that islet autoimmunity also targets neoepitopes expressed by the target cells, which may not be available for negative thymic selection. Differential expression of IA-2 and IGRP mRNAs in thymus and pancreas (157, 158) may promote autoimmunity, as the immune system may not be tolerant to alternatively spliced variants expressed in pancreas but not thymus (159). Many autoantigens in autoimmune disease are post-translationally modified (PTM) (160). Inflammation and stress are likely factors in the generation of PTM antigens, which derive from both normal and abnormal processes in cells. Predisposing HLA types are critical for the presentation of these epitopes to T cells (161, 162). Below, the major neoepitope classes associated with T1D are described.. Neoepitopes generated by PTM. A PTM epitope exists in the insulin A chain (A1-A13): T cell recognition requires oxidized cysteine residues at A6 and A7, with the formation of a vicinal disulfide bond between them (60). ...
Dear Immunonetters, I would like to bring another player into the Self/non-self discrimination arena. That Being the effect of Anergic T-cells on other autoreactive T-cells.This concept has been discussed in the papers by Lasalle and Hafler ( FASEB J. 8:601-608 1994) and Lombardi et al ( science 264:1587 1994). I agree with the authors that the Anergic T-cells play an important rolein self/nonself discrimination. In summary this is whats happening. The Thymus, site of clonal deletion, is very efficient in removing autoreactive T-cells. But nothing is perfect and some autoreactive cells escape this screening. These T-cells can be safely present in the periphery if the antigens they are reactive to are hidden away from them or not presented to them. This is called Clonal Ignorance. If MHC/AG is presented to the autoreactive T-cell but is not followed by costimulation, the result is Clonal anergy. In these cases the T-cells can recognize the self antigen however the extent of the response stops ...
T cell responses are essential for protection against pathogens but can also be detrimental to the host. Therefore many overlapping mechanisms exist to prevent both the development of autoimmunity and excessive tissue damage during chronic infections. T cell differentiation and effector function are shaped by the integration of different signals from the environment. These signals are orchestrated through a variety of signaling receptors including the T cell receptor, activating (co-stimulatory molecules or cytokines) and inhibitory (checkpoint) receptors. Thus, the modulation of external signals could impact on the development or function of effector and/or regulatory T (Treg) cells. In pre-clinical human or animal studies, the manipulation of T cell function has been attempted via numerous different approaches. These include (i) immune checkpoint blockade (PD-1, PD-L1, Tim3 and/or CTLA-4 among others), (ii) alterations in metabolic pathways and (iii) the utilization of biological agents such as
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Combination checkpoint blockade (CCB) targeting inhibitory CTLA4 and PD1 receptors holds promise for cancer therapy. Immune-related adverse events (IRAEs) remain a major obstacle for the optimal application of CCB in cancer. Here, we analyzed B cell changes in patients with melanoma following treatment with either anti-CTLA4 or anti-PD1, or in combination. CCB therapy led to changes in circulating B cells that were detectable after the first cycle of therapy and characterized by a decline in circulating B cells and an increase in CD21lo B cells and plasmablasts. PD1 expression was higher in the CD21lo B cells, and B cell receptor sequencing of these cells demonstrated greater clonality and a higher frequency of clones compared with CD21hi cells. CCB induced proliferation in the CD21lo compartment, and single-cell RNA sequencing identified B cell activation in cells with genomic profiles of CD21lo B cells in vivo. Increased clonality of circulating B cells following CCB occurred in some patients. ...
We offer a large selection of autoimmunity ELISA kits, it is vital that accurate and reliable assay methods are available to analyse autoimmune diseases for
Major Medline report on latest on causes and details of diabetes type 1 and type 2. Covers latest research on environmental causes of diabetes - details of autoimmunity process - and latest successes in reversing diabetes.
NK cells in CNS inflammation and autoimmunity Project Summary: Natural killer (NK) cells are large, granular lymphocytes that operate through cytolytic activity...
Current Research: My main interest is mechanistic dissection of natural and induced causes that precipitate the pathological state of the immune system, called autoimmunity. Autoimmunity generally clinically manifests as a variety of organ-specific diseases such as Type 1 Diabetes (T1D), for which we have a plethora of mouse models. Progression of T1D involves the activation of autoimmune T cells, consequent honing of activated lymphocytes to the pancreatic islets, and ensuing destruction of insulin-producing beta cells. Our studies focus on determining how autoimmune T cells are initially activated during T1D pathogenesis, how they hone to the target organ, and how they destroy their beta cell targets, causing clinical onset of T1D. The main goal of the research projects in my laboratory is to design and exploit tools for the manipulation of adaptive immunity for therapeutic purposes. To achieve this goal we use a variety of genetic, molecular biological, and biochemical approaches.. ...
Smith, H R.; Green, D; Raveche, E; Smathers, P; Gerson, R; and Steinberg, A D., The induction of autoimmunity in normal mice. Abstr. (1982). Subject Strain Bibliography 1982. 2071 ...
Scu has an interesting post up expanding on his discussion of Luhmann and vulnerability yesterday. It seems that he want to draw a distinction between immunity and autoimmunity as it works in Derridas thought. Im not entirely following what hes trying to get at here. As I understand it, the idea is that in order…
Autoimmunity is one of the subject in which we provide homework and assignment help. Our feature includes 24x7 live online statistics tutors available to help you. You can get speedy and cost Immunology help at assignmenthelp.net
Mellors, R C., (slow) Virus infection, autoimmunity, and and lymphoma, an experimental model of human disease. (1969). Subject Strain Bibliography 1969. 1878 ...
Last week I talked some general issues about autoimmunity, and gave a brief background on NKT cells. Today Ill talk about the paper that spawned that discussion. ((Mattner, J., Savage, P., Leung, P., Oertelt, S., Wang, V., Trivedi, O., Scanlon, S., Pendem, K., Teyton, L., Hart, J. (2008). Liver Autoimmunity Triggered
From a lecture in Sweden autumn 2014 Dr. Suzanne Humphries speaks on vaccines and autoimmunity. Is there a connection between vaccination and asthma and allergy? Also, aluminium is used as an adjuvant, how does this affect the human body? More about Dr. Suzanne Humphries: http://drsuzanne.net/ THIS IS A NON PROFIT VIDEO PRODUCTION. ALL DONATIONS ARE APPRECIATED. PayPal: [email protected] THANK YOU ! Canal 2nd Opinion Sweden http://www.2op.se https://www.facebook.com/pages/Canal-2nd-Opinion/260569270754045
HOW TO PREVENT ALLERGIES, AUTOIMMUNITY AND CANCER IN HUMANS AND IN ANIMALS Todays toxic world contains many different harmful, health invaders, that it is
Wei, W.,Ming, X.,Yi, Z. Y.,et al. Autoimmunity Mediated Down-regulation Of B 2-adrenergic Receptor In COPD[J]. AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE,2010,181 ...
AUTOIMMUNITY and HYPERINSULINEMIA related symptoms, diseases, and genetic alterations. Get the complete information with our medical search engine for
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Infections and autoimmunity: the multifaceted relationship: http://www.jleukbio.org/content/87/3/385.full This article mentioned RNase L, as well as...
Turning to efficient autoimmunity testing, tools can have major impact on a physicians diagnostic decision, making an equally major difference in patient care.
Written by: Greg Ashby Have you ever wondered about autoimmunity? What is it, anyway? Chances are that you know someone affected - maybe that person i(...)
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CD4+Foxp3+ regulatory T cells (Tregs) are known to control the progression of autoimmune diabetes, but when, where and how they exert their influence in this context are questions even now less than energetic controversy. afterwards. Interferon (IFN)- affected extensively on the gene-expression program of the local CD4+ effector cell population, unleashing it to aggressively attack the islets, and very HSP90AA1 crucial for the development of diabetes. Thus, Tregs rein in pancreatic autoimmunity through control of a central innate immune system player, NK cells. INTRODUCTION Foxp3+CD4+ Tregs Xanomeline oxalate manufacture regulate a variety of immune responses, including autoimmunity, allergy, inflammation, infection and tumorigenesis (Zheng and Rudensky, 2007; Sakaguchi et al., 2008). This cell population is required life-long to guard against autoimmunity, perhaps best illustrated by the multi-organ infiltrates that arise a few weeks after its acute ablation in adult mice (Kim et al., 2007). In ...
Low-level autoimmunity[edit]. While a high level of autoimmunity is unhealthy, a low level of autoimmunity may actually be ... a b Tolerance and Autoimmunity *^ Edwards JC, Cambridge G, Abrahams VM (1999). "Do self perpetuating B lymphocytes drive human ... Arthur M. Silverstein: Autoimmunity: A History of the Early Struggle for Recognition, in: Ian R. Mackay, Noel R Rose: The ... Nutrition and autoimmunity[edit]. Vitamin D/Sunlight *Because most human cells and tissues have receptors for vitamin D, ...
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Autoimmunity has been increasingly linked to targeted deregulation of epigenetic mechanisms, and therefore, use of epigenetic ... Research into the link between smell, depressive behavior, and autoimmunity has turned up interesting findings including the ... Sawalha A.H. (2008). "Epigenetics and T-cell immunity". Autoimmunity. 41 (4): 245-252. doi:10.1080/08916930802024145. PMID ... to autoimmunity and neurodegeneration. Other evidence has shown that development and deployment of the innate and acquired ...
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... form a regulatory T-cell population that protects self tissues from immune attack or autoimmunity. HLA-DQ (DQ) is encoded on ... Autoimmunity. 39 (4): 277-288. doi:10.1080/08916930600738581. PMID 16891216. S2CID 23462117. Fasano, Alessio (2011). "Dr". ... indicate that potentially a small change or increase in the presentation of a potential self-antigen can result in autoimmunity ...
snRNP70 Migliorini P, Baldini C, Rocchi V, Bombardieri S (February 2005). "Anti-Sm and anti-RNP antibodies". Autoimmunity. 38 ( ...
Böhm I (2003). "Disruption of the cytoskeleton after apoptosis induction by autoantibodies". Autoimmunity. 36 (3): 183-89. doi: ...
Tian J, Lu Y, Zhang H, Chau CH, Dang HN, Kaufman DL (2004). "Gamma-aminobutyric acid inhibits T cell autoimmunity and the ... Autoimmunity. 44 (6): 465-70. doi:10.3109/08916934.2011.571223. PMC 5787624. PMID 21604972. Bhandage AK, Jin Z, Korol SV, Shen ...
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"Autoimmunity". webMIC 419: Immunology. University of Arizona. Archived from the original on 2003-06-10. Green DR, Ware CF (June ... "Limited Peripheral T Cell Anergy Predisposes to Retinal Autoimmunity". The Journal of Immunology. 178 (7): 4276-4283. doi: ...
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February 2014). "Coxsackievirus B1 is associated with induction of β-cell autoimmunity that portends type 1 diabetes". Diabetes ... Stratton, Richard; Slapak, Gabrielle; Mahungu, Tabitha; Loes, Sabine Kinloch-de (2009). "Autoimmunity and HIV". Current Opinion ... Shapira, Yinon; Agmon-Levin, Nancy; Shoenfeld, Yehuda (2009). "Mycobacterium Tuberculosis, Autoimmunity, and Vitamin D". ... 2001). "Echovirus 4 and type 1 diabetes mellitus". Autoimmunity. 34 (4): 275-81. doi:10.3109/08916930109014696. PMID 11905853. ...
similima.com > Autoimmunity Archived 2011-07-27 at the Wayback Machine By Muhammed Muneer. Retrieved Mars 2011 "Archived copy ... Autoimmunity. 37 (1): 37-44. doi:10.1080/08916930310001630325. PMID 15115310. Li, Qing Kay; Khalbuss, Walid E. (2015). ...
1995). "Different HLA-DQ are positively and negatively associated in Swedish patients with myasthenia gravis". Autoimmunity. 22 ...
Su KY, Pisetsky DS (September 2009). "The role of extracellular DNA in autoimmunity in SLE". Scand. J. Immunol. 70 (3): 175-83 ... Blank M, Barzilai O, Shoenfeld Y (February 2007). "Molecular mimicry and auto-immunity". Clin Rev Allergy Immunol. 32 (1): 111- ... Autoimmunity. 39 (1): 63-70. doi:10.1080/08916930500484849. PMID 16455583. S2CID 9844130. Berden JH (August 2003). "Lupus ...
CS1 maint: discouraged parameter (link) Volpe, Robert (1989). "The Life of Doctor Hakaru Hashimoto". Autoimmunity. 3 (4): 243-5 ...
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This role could be used to prevent autoimmunity and to enhance memory responses after vaccination. Our understanding of the ... Baxter AG, Smyth MJ (February 2002). "The role of NK cells in autoimmune disease". Autoimmunity. 35 (1): 1-14. doi:10.1080/ ...
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Autoimmunity[edit]. There is an increasing number of studies indicating that POTS is an autoimmune disease.[47][50][51][52][53] ... "Antiadrenergic autoimmunity in postural tachycardia syndrome". Europace. 19 (7): 1211-1219. doi:10.1093/europace/euw154. PMC ... "Antiadrenergic autoimmunity in postural tachycardia syndrome". Europace. 19 (7): 1211-1219. doi:10.1093/europace/euw154. PMC ... "Autoimmunity in postural orthostatic tachycardia syndrome: Current understanding". Autonomic Neuroscience. Postural ...
Autoimmunity Reviews. 15 (6): 558-63. doi:10.1016/j.autrev.2016.02.010. PMID 26876385. Samson M, Puéchal X, Devilliers H, Ribi ... Autoimmunity Reviews. 13 (9): 945-53. doi:10.1016/j.autrev.2014.08.002. PMID 25153486. Hellmann DB, Laing TJ, Petri M, Whiting- ...
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Shelly, S.; Boaz, M.; Orbach, H. (2012). "Prolactin and autoimmunity". Autoimmunity Reviews. 11 (6-7): A465-A470. doi:10.1016/j ...
Islam, Md Asiful (2018). "Antiphospholipid Antibodies in Epilepsy: A Systematic Review and Meta-analysis". Autoimmunity Reviews ... Autoimmunity Reviews. 17 (3): 226-243. doi:10.1016/j.autrev.2017.10.014. PMID 29355608 - via Science Direct. "Aps , Action". ... Autoimmunity Reviews. 16 (5): 512-522. doi:10.1016/j.autrev.2017.03.005. PMID 28279839 - via Science Direct. ... Autoimmunity Reviews. 18 (9): 102352. doi:10.1016/j.autrev.2019.102352. PMID 31323355. Islam, Md Asiful (2016). " ...
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This autoimmunity called IPEX is an attack from the body's own immune system against the body's own tissues and organs. Early ... It leads to the dysfunction of CD4+ regulatory T-cells and the subsequent autoimmunity. The disorder is one of the autoimmune ... Kitcharoensakkul, Maleewan; Cooper, Megan A. (2020-01-01), Rose, Noel R.; Mackay, Ian R. (eds.), "Chapter 28 - Autoimmunity in ... a paradigm of immunodeficiency with autoimmunity". Frontiers in Immunology. 3: 211. doi:10.3389/fimmu.2012.00211. PMC 3459184. ...
Autoimmunity Reviews. 11 (9): 636-41. doi:10.1016/j.autrev.2011.11.004. PMID 22100329. Beltran AS, Russo A, Lara H, Fan C, ...
Infection, autoimmunity, and vitamin D. eds. Shoenfeld Y, Rose NR. Infection and autoimmunity. 2014; 163-82. ... The human microbiome and autoimmunity. Curr Opin Rheumatol. 2013 Mar;25(2):234-40. doi: 10.1097/BOR.0b013e32835cedbf. PubMed ... Re-framing the Theory of Autoimmunity in the Era of the Microbiome: Persistent Pathogens, Autoantibodies, and Molecular Mimicry ...
Autoimmunity is an international, peer-reviewed medical journal that covers the pathogenesis, immunology, genetics, and ... The editor in chief of Autoimmunity is Paolo Casali, the Donald L Bren Professor of Medicine, Molecular Biology & Biochemistry ... "About Autoimmunity". Retrieved 2010-01-20. "Paolo Casali Homepage". Retrieved 2010-01-20.. ...
Thymoma-associated multiorgan autoimmunity (TAMA) is a severe often fatal disease that presents in some patients with thymoma. ... Wadhera A, Maverakis E, Mitsiades N, Lara PN, Fung MA, Lynch PJ (Oct 2007). "Thymoma-associated multiorgan autoimmunity: a ...
Low-level autoimmunity[edit]. While a high level of autoimmunity is unhealthy, a low level of autoimmunity may actually be ... a b Tolerance and Autoimmunity *^ Edwards JC, Cambridge G, Abrahams VM (1999). "Do self perpetuating B lymphocytes drive human ... Arthur M. Silverstein: Autoimmunity: A History of the Early Struggle for Recognition, in: Ian R. Mackay, Noel R Rose: The ... Nutrition and autoimmunity[edit]. Vitamin D/Sunlight *Because most human cells and tissues have receptors for vitamin D, ...
... Autoimmunity. The immune system defends the body against infections and certain other diseases. It is ... This is called autoimmunity. One example of an autoimmune disease is type 1 diabetes, in which the immune system destroys the ...
Multisystem autoimmunity Immunity consists of innate and adaptive responses. Innate immune systems are found in all classes of ... Zenewicz LA, Abraham C, Flavell RA, Cho JH (2010) Unraveling the genetics of autoimmunity. Cell 140:791-797PubMedCentralPubMed ... Pollard K.M. (2016) Systemic Autoimmunity. In: Vohr HW. (eds) Encyclopedia of Immunotoxicology. Springer, Berlin, Heidelberg. * ... Mechanisms of environmental influence on human autoimmunity: a National Institute of Environmental Health Sciences expert panel ...
... * Green Cleaning: Exposure ... This population has a high prevalence of autoimmunity, particularly systemic lupus erythematosus (SLE). Additionally, locally ... The partnership studied the link between these persistent organic pollutants and autoimmunity. ... with the Sea Island Families Project Advisory Committee to determine whether environmental exposures trigger autoimmunity and ...
Allergies/autoimmunity. Category archives for Allergies/autoimmunity. UCS response to my piece in SciAm. Posted by Kevin Bonham ... OAS Wednesday - Activating immunity to suppress autoimmunity.. Posted by Kevin Bonham on May 15, 2013 ...
Purchase Cancer and Autoimmunity - 1st Edition. Print Book & E-Book. ISBN 9780444503312, 9780080528458 ... Autoimmunity in B-Lymphoproliferative Disorders (Viggo Jonsson, Allan Wiik).. *CD5 Positive B Cells: Crossroads of Autoimmunity ... Chapter IV: Therapy in Autoimmunity and Cancer - Common and Different Denominators.. *Therapy of Cancer and Autoimmunity: ... "Autoimmunity Reviews" (Elsevier) (Impact factor 7.9) and Co-Editor of "Journal of Autoimmunity" (Impact factor 8.1). He has ...
The epigenetics of autoimmunity.. Meda F1, Folci M, Baccarelli A, Selmi C. ... settings and experimental models proposed that the epigenome may hold the key to a better understanding of autoimmunity ... support other complementary mechanisms involved in the regulation of genes expression ultimately causing overt autoimmunity. ...
"For that reason, we believe it is affecting a basic mechanisms of autoimmunity." The researchers do not know how the ... Earlier work had suggested that EBV might promote the development of autoimmunity. "We were completely surprised. So, we redid ... "Epstein Barr Virus Protects Against Autoimmunity." Medical News Today. MediLexicon, Intl., 4 Apr. 2012. Web.. 19 Jan. 2019. , ... Health, N. (2012, April 4). "Epstein Barr Virus Protects Against Autoimmunity." Medical News Today. Retrieved from. https://www ...
... Aristo Vojdani. ,1 K. Michael Pollard. ,2 and Andrew W. Campbell3. 1Immunosciences ... show that the effect of DAF on autoimmunity is complex and may require multiple genetic elements such as a tandem repeat ... The author discusses the importance of early detection of autoimmunity via antibody testing to bring about a better outcome for ... Further understanding of this novel mechanism by which DAF can regulate mercury-induced autoimmunity may lead to new strategies ...
... by: ISBN: 0-7414-1792-8 ©2003. Price: $11.95 Book Size: 5.5 x 8.5 , 139 pages. Category/Subject ... Autoimmunity and hypersensitivity can cause an immune system to become a persons own worst enemy. If someone knows that ... autoimmunity or hypersensitivity is causing the distress, damage can be prevented. Lives can be saved! Millions suffer from ...
CRYs regulate autoimmunity. Qi Cao, Xuan Zhao, Jingwen Bai, Sigal Gery, Haibo Sun, De-Chen Lin, Qi Chen, Zhengshan Chen, Lauren ... CRYs regulate autoimmunity. Qi Cao, Xuan Zhao, Jingwen Bai, Sigal Gery, Haibo Sun, De-Chen Lin, Qi Chen, Zhengshan Chen, Lauren ... Circadian clock cryptochrome proteins regulate autoimmunity. Qi Cao, Xuan Zhao, Jingwen Bai, Sigal Gery, Haibo Sun, De-Chen Lin ... B cell-mediated autoimmunity is frequently linked to the hyperactivation of B cells. In this regard, mice deficient in the ...
Autoimmunity. Say: aw-toh-ih-myoo-nih-tee. Your immune system fights infections and illnesses. It prevents you from getting ... This is called autoimmunity. One example of an autoimmune disease is type 1 diabetes, in which the immune system destroys the ...
Our Autoimmunity, Transplantation & Inflammation (ATI) disease team is at the forefront of translational science revealing how ...
... and clinical studies on all aspects of autoimmunity. As a multidisciplinary journal, basic science aimed at understanding the ... Autoimmunity Diseases of the Skin. Jozélio Freire Carvalho,1 Paulo Ricardo Criado,2 Valéria Aoki,2 and Yehuda Shoenfeld3 ... Autoimmunity Reviews, vol. 12, pp. 121-126, 2012. View at Publisher · View at Google Scholar ... Autoimmunity Reviews, vol. 12, pp. 599-606, 2013. View at Publisher · View at Google Scholar ...
Autoimmunity may also involve dysregulation of genes or pathways regulated by the RUNX family of transcription factors. RUNX is ... The genetics of psoriasis and autoimmunity.. Bowcock AM1.. Author information. 1. Department of Genetics, Washington University ...
Approach targets autoimmunity. At a Glance. *Researchers developed a strategy to treat a rare autoimmune disease called ... including autoimmunity and transplant rejection," Milone says. ... The Origins of Autoimmunity-Causing T Cells. *Technique Directs ...
Principal Investigator, Inflammation and Autoimmunity Tel 984-287-4089 [email protected] Curriculum Vitae Jennifer ... The Inflammation and Autoimmunity Group is centered on understanding how the autophagy machinery regulates inflammation and ... Jennifer Martinez, Ph.D. heads the Inflammation and Autoimmunity Group, and holds a secondary appointment in the NIEHS Signal ... This research performed in the Inflammation and Autoimmunity Group has garnered national and international recognition, in the ...
Cite this: Attacking Autoimmunity Through the Gut: Folly or Science? - Medscape - Oct 24, 2019. ... The goal is to lower inflammation, which is recognized as the underlying pathologic mechanism behind autoimmunity. ... Despite growing recognition that leaky gut triggers many illnesses, including autoimmunity, there is surprisingly little ... only a percentage of people with autoimmunity can benefit from the diet. We do not have validated biomarkers for non-celiac ...
Autoimmunity * Sexual dimorphism in autoimmunity Kira Rubtsova et al. * Checkpoints that control B cell development Fritz ... Mechanisms of human autoimmunity Michael D. Rosenblum et al. * T cells in the control of organ-specific autoimmunity Jeffrey A ... Genetic basis of autoimmunity Alexander Marson et al. * MicroRNA regulation of lymphocyte tolerance and autoimmunity Laura J. ... Mechanisms of human autoimmunity. J Clin Invest. 2015;125(6):2228-2233.. View this article via: JCI Google Scholar ...
... structured reviews on diverse topics in autoimmunity, written by first-class experts in the field. The... ... Autoimmunity Reviews will publish up-to-date, structured reviews on diverse topics in autoimmunity, written by first-class ... Autoimmunity Reviews will publish up-to-date, structured reviews on diverse topics in autoimmunity, written by first-class ... Special issues published in Autoimmunity Reviews. * 9th International Congress on Autoimmunity in Nice Carlo Perricone , ...
The Journal of Autoimmunity is a parent journal of the Journal of Translational Autoimmunity. The Journal of Autoimmunity ... The Journal of Autoimmunity is a parent journal of the Journal of Translational Autoimmunity. The Journal of Autoimmunity ... The Journal of Autoimmunity is a parent journal of the Journal of Translational Autoimmunity. The Journal of Autoimmunity ... Liver Autoimmunity: Paradigm versus Paradox and Breach of Tolerance Benedetta Terziroli Beretta-Piccoli , Diego Vergani ...
Low-level autoimmunityEdit. While a high level of autoimmunity is unhealthy, a low level of autoimmunity may actually be ... For journal, see Autoimmunity (journal).. Autoimmunity is the system of immune responses of an organism against its own healthy ... a b Tolerance and Autoimmunity. *^ Edwards JC, Cambridge G, Abrahams VM (1999). "Do self perpetuating B lymphocytes drive human ... Arthur M. Silverstein: Autoimmunity: A History of the Early Struggle for Recognition, in: Ian R. Mackay, Noel R Rose: The ...
Gut microbe drives autoimmunity. At a Glance. *Scientists found evidence that a certain gut microbe can trigger autoimmune ... References: Translocation of a gut pathobiont drives autoimmunity in mice and humans. Manfredo Vieira S, Hiltensperger M, Kumar ... as vaccinations against other bacteria we investigated did not prevent mortality and autoimmunity," Kriegel says. "Treatment ...
Autoimmunity, Infection and Cancer - 1st Edition. Print Book & E-Book. ISBN 9780444828071, 9780080534435 ... "Autoimmunity Reviews" (Elsevier) (Impact factor 7.9) and Co-Editor of "Journal of Autoimmunity" (Impact factor 8.1). He has ... Idiotypes in Medicine: Autoimmunity, Infection and Cancer 1st Edition. Write a review ... "The Mosaic of Autoimmunity", "Infections and Autoimmunity" and the textbook "Autoantibodies" and "Diagnostic criteria of ...
Other T-cells can suppress or enhance autoimmunity (either in general or only for T lymphocytes in islets). The activation of a ... When a T-cell is activated through its receptor, it can orchestrate protection from infection or autoimmunity, depending on the ...
POSTDOCTORAL POSITIONS IN AUTOIMMUNITY -Forwarded. Andras Perl PERLA at MAILBOX.HSCSYR.EDU Thu Mar 12 07:19:40 EST 1998 * ...
The higher prevalence of autoimmunity among women at child-bearing ages, disease onset/relapses during pregnancy and post- ... The higher prevalence of autoimmunity among women at childbearing ages, disease onset/relapses during pregnancy, and post- ... of autoimmune diseases between genders represents one of the most enigmatic observations among the mosaic of autoimmunity. Sex ... of autoimmune diseases between genders represents one of the most enigmatic observations among the mosaic of autoimmunity. Sex ...
  • Re-framing the Theory of Autoimmunity in the Era of the Microbiome: Persistent Pathogens, Autoantibodies, and Molecular Mimicry. (autoimmunityresearch.org)
  • Children with multiple islet autoantibodies - biological markers of autoimmunity -- are more likely to progress to symptomatic type 1 diabetes (T1D) than those who remain positive for a single autoantibody. (news-medical.net)
  • Blood samples taken every 3 months were used to test for the appearance of 1 or more of the islet autoantibodies GADA, IAA, or IA-2A, as markers for islet autoimmunity. (medscape.com)
  • One common type of autoimmunity is when the immune system makes antibodies against normal cells and/or tissues of the body which are known as "autoantibodies. (primaryimmune.org)
  • A few obese youth with type 2 diabetes have evidence of islet cell autoimmunity with autoantibodies toward β-cells typical of type 1 diabetes defining what is called "double diabetes" (DD). (diabetesjournals.org)
  • The serological presence of autoantibodies is diagnostic of autoimmunity, and these autoantibodies may be present for many years before the presentation of autoimmune disease (AID). (mdpi.com)
  • Whittingham, S.F. The Role of Pathogenic Autoantibodies in Autoimmunity. (mdpi.com)
  • He has written more than three hundred and fifty chapters in books, and has authored and edited 25 books, some of which became cornerstones in science and clinical practice, such as "The Mosaic of Autoimmunity", "Infections and Autoimmunity" and the textbook "Autoantibodies" and "Diagnostic criteria of autoimmune diseases", all of which were published by Elsevier and sold by the thousands. (google.ch)
  • The Journal of Autoimmunity is a parent journal of the Journal of Translational Autoimmunity . (elsevier.com)
  • He is on the editorial board of 43 journals in the field of rheumatology and autoimmunity and is the founder and the editor of the IMAJ (Israel Medical Association Journal) the representative journal of science and medicine in the English language in Israel, and also is the founder and Editor of the "Autoimmunity Reviews" (Elsevier) (Impact factor 7.9) and Co-Editor of "Journal of Autoimmunity" (Impact factor 8.1). (google.ch)
  • The Journal of Autoimmunity publishes papers related to the diverse aspects of autoimmunity: the mechanism of self-recognition, regulation of autoimmune responses, experimental autoimmune diseases, diagnostic autoantibody tests, and the epidemiology, pathophysiology, and treatment of autoimmune diseases. (scimagojr.com)
  • Autoimmunity is an international, peer-reviewed medical journal that covers the pathogenesis, immunology, genetics, and molecular biology of immune and autoimmune responses. (wikipedia.org)
  • Is autoimmunity involved in pathogenesis of autism? (autismspeaks.org)
  • Autoimmunity and the pathogenesis of myocarditis. (ahajournals.org)
  • This Program Announcement (PA), Mechanism of Gender's Effect in Pathogenesis of Autoimmunity, is related to the priority area of diabetes and chronic disabling diseases. (nih.gov)
  • Additional factors may play a role in the disease pathogenesis, and may promote β-cell dysfunction and progression of islet autoimmunity. (diabetesincontrol.com)
  • The great asymmetry of autoimmune diseases between genders represents one of the most enigmatic observations among the mosaic of autoimmunity. (frontiersin.org)
  • Gender dimorphism represents one of the most enigmatic observations among the mosaic of autoimmunity. (frontiersin.org)
  • Rates and Deadlines listed below are for the 2018-E4 "B Cells: Mechanisms in Immunity and Autoimmunity" conference only. (keystonesymposia.org)
  • For that reason, we believe it is affecting a basic mechanisms of autoimmunity. (medicalnewstoday.com)
  • The mechanisms of autoimmunity suppression by regulatory T-cells are widely studied. (innovations-report.com)
  • At the root of the diet is the theory that intestinal barrier dysfunction, or leaky gut , is allowing toxins into the system, triggering inflammation and autoimmunity. (medscape.com)
  • The lecture will focus on inflammation and autoimmunity and will include an opportunity to book an initial appointment with the practitioner. (eventbrite.com)
  • "For several years there has been controversy among scientists about whether vitamin D lowers the risk of developing of islet autoimmunity and type 1 diabetes," ​commented lead author Dr Jill Norris from the Colorado School of Public Health. (nutraingredients.com)
  • Graves' disease is a type of autoimmunity in which the thyroid gland becomes overly active. (everydayhealth.com)
  • Association between thyroid autoimmunity and recurrent angioedema. (ingentaconnect.com)
  • The association between thyroid autoimmunity (TA) and idiopathic isolated angioedema (or angioedema without urticaria) has not been evaluated in either children or in adults up until now. (ingentaconnect.com)
  • It is likely that thyroid autoimmunity might be more frequent in the adult acne patients and this should be kept in mind when screening women with post-adolescent acne. (nih.gov)
  • Increase prevalence of thyroid autoimmunity is found in patients with chronic urticaria. (clinicaltrials.gov)
  • About 5-34% of chronic urticaria patients is associated with the presence of thyroid autoimmunity who are euthyroid status whereas 5-10% of them with either hyperthyroidism or hypothyroidism. (clinicaltrials.gov)
  • This study is designed to investigate the prevalence of thyroid autoimmunity associated with chronic urticaria in Taiwanese population. (clinicaltrials.gov)
  • In addition, we intend to find out the change in the level of thyroid autoimmunity after the treatment in order to further understand their relationship. (clinicaltrials.gov)
  • We also intend to find out the prognostic parameters in patients with the presence of thyroid autoimmunity and chronic urticaria. (clinicaltrials.gov)
  • show that the effect of DAF on autoimmunity is complex and may require multiple genetic elements such as a tandem repeat sequence (CTTTT)n or (TTTTC)n. (hindawi.com)
  • Infants who are at genetic risk of developing type 1 diabetes and who were given probiotics before 3 months of age had a 33% reduction in the risk of pancreatic beta-cell islet autoimmunity, according to new results from an ongoing international study in over 7000 children. (medscape.com)
  • Ensuring good levels of vitamin D throughout infancy could be vital to lowering the risk of autoimmunity in children at genetic risk for type 1 diabetes, say researchers. (nutraingredients.com)
  • In the current study, Norris and colleagues compared 376 children who developed islet autoimmunity with 1,041 children who did not - finding that in children with a genetic variant in the vitamin D receptor gene, vitamin D levels in infancy and childhood were lower in those that went on to develop islet autoimmunity compared with those that did not develop autoimmunity. (nutraingredients.com)
  • Not everyone develops autoimmunity - there may be a genetic susceptibility. (drmyhill.co.uk)
  • Celiac disease and endocrine autoimmunity do share a common genetic background, which definitely explains some of the relationship. (celiac.com)
  • In addition, the volume contains critical updates on autoimmunity, organ transplantation, tumor immunology and genetic mouse models for mechanistic studies. (springer.com)
  • The editor in chief of Autoimmunity is Paolo Casali, the Donald L Bren Professor of Medicine, Molecular Biology & Biochemistry and Director of the Institute for Immunology at the University of California at Irvine. (wikipedia.org)
  • An invitation to convene a symposium on autoimmunity in Berlin warrants a célébration of one of the principal architects of immunology, Paul Ehrlich. (springer.com)
  • Pollard K.M. (2016) Systemic Autoimmunity. (springer.com)
  • As chief of the Systemic Autoimmunity Branch, she works to identify mechanisms of organ damage and premature vascular disease in systemic autoimmunity. (nih.gov)
  • The broad and long-term objectives of the Systemic Autoimmunity Branch are to further the understanding of the clinical spectrum and pathophysiology of systemic autoimmune diseases, and to translate this knowledge into better therapies that improve outcomes for patients with these conditions. (nih.gov)
  • A major goal of the Systemic Autoimmunity Branch is to combine natural history or treatment studies with basic investigations into the etiology and/or pathophysiology of rheumatic diseases, with an emphasis on SLE, AAV, RA and other systemic autoimmune diseases affecting adults. (nih.gov)
  • Here we show that T cell-restricted Srsf1-deficient mice develop systemic autoimmunity and lupus-nephritis. (jci.org)
  • In the investigation led by Dr. Uusitalo, the researchers wanted to test the hypothesis that early probiotic exposure might be associated with reduced risk for islet-cell autoimmunity. (medscape.com)
  • Islet-cell autoimmunity was found in 575 infants, 7.7% of the total. (medscape.com)
  • The increasingly "obesogenic" environment that favors insulin resistance could account for the development of islet cell autoimmunity through different mechanisms. (diabetesjournals.org)
  • This study defines a population that may be susceptible to post-vaccination autoimmunity, termed autoimmune syndrome induced by adjuvants (ASIA). (greenmedinfo.com)
  • Predicting post-vaccination autoimmunity: Who might be at risk? (sanevax.org)
  • Autoimmunity may also involve dysregulation of genes or pathways regulated by the RUNX family of transcription factors. (nih.gov)
  • This can lead to autoimmunity, one form of immune dysregulation in which the immune response is directed against normal parts of the body such as cells, tissues or organs (called auto-antigens). (primaryimmune.org)
  • The focus of this chapter is to provide an overview of the types of immune dysregulation and autoimmunity that can occur in various primary immunodeficiency diseases. (primaryimmune.org)
  • Autoimmunity results from the dysregulation of the immune system leading to tissue damage. (ingentaconnect.com)
  • These could even precede the triggering of islet autoimmunity, and may promote chronic immune dysregulation through effects on both innate and adaptive immune responses. (diabetesincontrol.com)
  • The higher prevalence of autoimmunity among women at childbearing ages, disease onset/relapses during pregnancy, and post-partum are some of the arguments that support this hypothesis. (frontiersin.org)
  • He describes the effects of dietary components, focusing particularly on recent studies with sodium chloride to explain the effects of this commonly used mineral on the immune system, in particular TH17, leading to an increased risk of autoimmunity. (hindawi.com)
  • However, very little is known about the influence of smoking in this regard, and how it may lead to autoimmunity. (ki.se)
  • Nearly 3,000 doctors and scientists from around the world gathered last week at the 9th International Congress on Autoimmunity (ICA) in the Nice Acropolis Convention Center on the French Riviera. (greenmedinfo.com)
  • QIAGEN provides a broad range of assay technologies for inflammatory response and autoimmunity research that enables analysis of gene expression and regulation, epigenetic modification, genotyping, and signal transduction pathway activation. (qiagen.com)
  • Deficiency of the Effector Mechanisms of the Immune Response and Autoimmunity (P. Lachmann & M. Walport). (wiley.com)
  • ASIA is also dubbed "Schoenfeld's Syndrome" for Schoenfeld who has published more than 1,700 articles in the medical literature and is widely regarded as the world's leading authority on autoimmunity -- disease that results when certain proteins in the body lose their "immune privilege" or protected status, and the machinery of the human defence system mistakes them as foreign invaders and launches an assault on its own body. (greenmedinfo.com)
  • He is considered a pioneer in his field and an international authority on autoimmunity and autism. (latitudes.org)
  • Shoenfeld Y, Rose NR. Infection and autoimmunity . (autoimmunityresearch.org)
  • Infection and Autoimmunity encompasses the different mechanisms involved in the infection-autoimmunity association/induction. (google.ch)
  • For the first time, scientists have found evidence that autoimmunity may have a role in Parkinson's disease. (medicalnewstoday.com)
  • Similarly, we provide evidence that autoimmunity against specific M2AChR epitopes (M2AChR-el2 and M2AChR-il3) may play a causal role in DCM. (bartleby.com)
  • Earlier work had suggested that EBV might promote the development of autoimmunity. (medicalnewstoday.com)
  • Importantly, therapeutic intervention in NOD mice through nutritional supplementation or lentivirus-mediated expression of an ω-3 fatty acid desaturase, m fat- 1, normalized blood glucose and insulin levels for at least 182 days, blocked the development of autoimmunity, prevented lymphocyte infiltration into regenerated islets, and sharply elevated the expression of the β cell markers pancreatic and duodenal homeobox 1 ( Pdx1 ) and paired box 4 ( Pax4 ). (jci.org)
  • Our Autoimmunity, Transplantation & Inflammation (ATI) disease team is at the forefront of translational science revealing how and why the immune system malfunctions. (novartis.com)
  • The persistence and/or reactivation of islet autoimmune responses is an obstacle to curing diabetes through transplantation, and autoimmunity may not be completely controlled by the immunosuppression used to prevent transplant rejection [76]. (diabetesincontrol.com)
  • The mTOR complex 1 (mTORC1) inhibitor rapamycin suppressed proinflammatory cytokine production by T cells and alleviated autoimmunity in Srsf1-deficient mice. (jci.org)
  • Rapamycin treatment reduces proinflammatory cytokine production by T cells and alleviates autoimmunity in Srsf1 -cKO mice. (jci.org)
  • More recently it has become accepted that autoimmune responses are an integral part of vertebrate immune systems (sometimes termed "natural autoimmunity"), [3] normally prevented from causing disease by the phenomenon of immunological tolerance to self-antigens . (wikipedia.org)
  • Second, autoimmunity may have a role in allowing a rapid immune response in the early stages of an infection when the availability of foreign antigens limits the response (i.e., when there are few pathogens present). (wikipedia.org)
  • Second, autoimmunity is likely to have a role in allowing a rapid immune response in the early stages of an infection when the availability of foreign antigens limits the response (i.e., when there are few pathogens present). (wikidoc.org)
  • Autoimmunity to antigens in pancreatic islets contributes to type 1 diabetes and thus control of this process has been of particular interest. (sciencemag.org)
  • The latter concept has been termed natural autoimmunity . (wikidoc.org)
  • This aspect may reflect possible commonalities of some pathogenetic events - even when triggered or sustained by distinct factors - that facilitate the progression from reversible loss of self-tolerance to chronic autoimmunity. (jci.org)
  • There is also evidence suggesting the co-existence of some low level of regeneration with chronic autoimmunity [81], as islet autoimmunity may also persist or perhaps be reactivated years after diagnosis. (diabetesincontrol.com)
  • What's the Relationship Between Celiac Disease and Endocrine Autoimmunity? (celiac.com)
  • A team of researchers recently set out to examine the relationship between celiac disease and endocrine autoimmunity. (celiac.com)
  • Our study effectively opens up the application of this anti-cancer technology to the treatment of a much wider range of diseases, including autoimmunity and transplant rejection," Milone says. (nih.gov)
  • The therapeutic part focusses on harnessing anti-idiotypes for treating autoimmunological disorders, and on the employment of idiotypes for vaccines in cancer and infectious diseases, as well as explaining the manipulation of the idiotypic network in autoimmunity and cancer idiotypes and vaccines. (elsevier.com)
  • Interestingly, recent evidence also indicates that other chronic inflammatory skin diseases and autoinflammatory syndromes, such as psoriasis, atopic dermatitis, lichen planus and localized scleroderma, are also (at least partially) caused by underlying autoimmunity. (frontiersin.org)
  • The American Autoimmune Related Diseases Association is dedicated to the eradication of autoimmune diseases and the alleviation of suffering and the socioeconomic impact of autoimmunity through fostering and facilitating collaboration in the areas of education, public awareness, research, and patient services in an effective, ethical and efficient manner. (aarda.org)
  • This grant from the National Institutes of Health's National Institute of Allergy and Infectious Diseases will fund research to understand why the immune system attacks its own body, referred to as compromised tolerance, and how autoimmunity develops. (news-medical.net)
  • Taking the experience of a beneficial factor in autoimmunity further, one might hypothesize with intent to prove that autoimmunity is always a self-defense mechanism of the mammal system to survive. (wikipedia.org)
  • The author discusses the loss of immune homeostasis and explains the mechanism of autoimmunity as related to infectious triggers by molecular mimicry, epitope spreading, and bystander activation. (hindawi.com)
  • Mechanism for the induction of autoimmunity and neuroautoimmunity by environmental triggers. (hindawi.com)
  • Further understanding of this novel mechanism by which DAF can regulate mercury-induced autoimmunity may lead to new strategies for regulation of DAF in various autoimmunities induced by environmental toxicants. (hindawi.com)
  • The goal is to lower inflammation, which is recognized as the underlying pathologic mechanism behind autoimmunity. (medscape.com)
  • Based on the obtained results we've discribed a new, previously unknown mechanism of autoimmunity regulation based on physiological ageing of immune cells and the activation of their self-destruction processes. (innovations-report.com)
  • The findings, published in Diabetes, ​examined the association between plasma levels of vitamin D -measured as 25-hydroxyvitamin D (25[OH]D) concentration - and islet autoimmunity(IA), which has been implicated in the development and progression of type 1 diabetes. (nutraingredients.com)
  • While it has long been known that islet autoimmunity - which occurs when the immune system attacks the islet cells in the pancreas that produce insulin - is a precursor to type 1 diabetes, evidence for the suggestion that vitamin D levels may play a role in the development of this autoimmunity, and therefore the progression of type 1 diabetes, has been mixed. (nutraingredients.com)
  • In this new study, the authors analysed whether the presence of enteroviruses in stools was associated with the appearance of islet autoimmunity in the "Type 1 Diabetes Prediction and Prevention Study" in Finland. (eurekalert.org)
  • The pathogenic role of idiotypes in autoimmunity and cancer is reviewed in depth. (elsevier.com)
  • These results implicate Pten in the Fas response and suggest that it may play a role as a suppressor of autoimmunity as well as cancer. (sciencemag.org)
  • We report that deletion of αv in the immune system causes severe colitis, autoimmunity, and cancer. (pnas.org)
  • First, low-level autoimmunity might aid in the recognition of neoplastic cells by CD8+ T cells , and thus reduce the incidence of cancer. (wikidoc.org)
  • Time that passes before first appearance of Opportunistic Autoimmunity Secondary to cancer Immunotherapy. (clinicaltrials.gov)
  • The 2020 Montagna Symposium on the Biology of Skin: Microbes, Autoimmunity and Cancer, focuses on exploring the interconnectedness and differences of the immune system throughout the body, and their interactions with viruses, bacteria and fungi that contribute to health and disease. (constantcontact.com)
  • In light of the discovery of Autoimmune Syndrome Induced by Adjuvants, or ASIA, Vaccines and Autoimmunity explores the role of adjuvants - specifically aluminum in different vaccines - and how they can induce diverse autoimmune clinical manifestations in genetically prone individuals. (wiley.com)
  • Edited by leaders in the field, Vaccines and Autoimmunity is an invaluable resource for advanced students and researchers working in pathogenic and epidemiological studies. (wiley.com)
  • Authors: Luísa Eça Guimarãesa, Britain Bakera, Carlo Perriconeb, Yehuda Shoenfelda,c Abstract Vaccines and autoimmunity are linked fields. (sanevax.org)
  • Some chapters follow discussing the vaccination and vaccines, including the controversial issue of vaccine-autoimmunity relationship. (google.ch)
  • The goal of this work is to better understand how the natural limitations of thymic selection predispose us to autoimmunity. (news-medical.net)
  • These lines of evidence strongly support other complementary mechanisms involved in the regulation of genes expression ultimately causing overt autoimmunity. (nih.gov)
  • discussed the relationship between DAF1 and the complement system in the regulation of environmentally induced autoimmunity. (hindawi.com)
  • Here, we report that αv integrins are central to the normal regulation of immune responses in the intestine and that deletion of αv in the immune system leads to spontaneous colitis, wasting, and autoimmunity. (pnas.org)
  • Researchers have identified functional single nucleotide polymorphisms of various genes involved in immune regulation as susceptibility genes for both celiac disease and monoglandular or polyglandular autoimmunity. (celiac.com)
  • Zenewicz LA, Abraham C, Flavell RA, Cho JH (2010) Unraveling the genetics of autoimmunity. (springer.com)
  • The genetics of psoriasis and autoimmunity. (nih.gov)
  • A team of researchers recently set out to determine whether there might exist ethnic differences in celiac disease autoimmunity in children at 6 years of age, and if present, to assess how these differences may be explained by known sociodemographic and environmental factors. (celiac.com)
  • Patients with monoglandular and/or polyglandular autoimmunity, and their relatives, have higher rates of celiac disease than those without such autoimmunity. (celiac.com)
  • Our aim was to investigate whether psychological stress, measured as psychosocial strain in families, is associated with diabetes-related autoimmunity during infancy. (diabetesjournals.org)
  • 0.01) were associated with diabetes-related autoimmunity in the child, independent of family history of diabetes. (diabetesjournals.org)
  • CONCLUSIONS - Psychological stress, measured as psychosocial strain in the family, seems to be involved in the induction, or progression, of diabetes-related autoimmunity in the child during the 1st year of life. (diabetesjournals.org)
  • We hypothesized that psychological factors may not only precipitate diabetes, but may also trigger or promote the progress of diabetes-related autoimmunity. (diabetesjournals.org)
  • Thus, islet autoimmunity may be active for many years, throughout the diabetes clinical spectrum (Figure 29.2), and not just limited to the time prior to and around diagnosis. (diabetesincontrol.com)
  • Special attention is given to heat shock proteins (HSPs) and to transgenic mouse models to better understand infection-induced autoimmunity. (google.ch)
  • Autoimmunity takes place when lymphocytes become activated by peptides derived from the body's own proteins rather than those from pathogens, activating an immune response. (news-medical.net)
  • Recent studies show that inappropriate levels of these cell types can occur during pathological conditions, potentially causing autoimmunity. (qiagen.com)
  • The Human Inflammatory Response & Autoimmunity miScript miRNA PCR Array profiles the expression of 84 miRNAs predicted to regulate the expression of proinflammatory or antiinflammatory genes. (qiagen.com)
  • This experiment will investigate whether the mechanisms which regulate autoimmunity are inadequate in children with autism and whether this is accompanied by signs of immune system activation. (autismspeaks.org)
  • The registry was established in January of this year as a tool to enable researchers to analyze cases of ASIA globally, to compare clinical manifestations after exposure, and to establish common instigators of autoimmunity and compare efficacy of treatments. (greenmedinfo.com)
  • Importantly, insulin resistance precedes T1DM diagnosis and accelerates the progression of islet autoimmunity [85-88]. (diabetesincontrol.com)
  • In recent years, several studies both in clinical settings and experimental models proposed that the epigenome may hold the key to a better understanding of autoimmunity initiation and perpetuation. (nih.gov)
  • Asked to comment on the data, Outi Vaarala, MD, research director at the Institute of Clinical Medicine, University of Helsinki, Finland, said: "The results of the study by Dr. Uusitalo, if reproduced in another observational study, suggest that an intervention with probiotics could be reasonable for the prevention of beta-cell autoimmunity. (medscape.com)
  • Neuromyelitis optica (NMO) is often associated with other clinical or serological markers of non-organ-specific autoimmunity. (nih.gov)
  • Autoimmunity is the failure of an organism to recognize its own constituent parts (down to the sub-molecular levels) as self , which results in an immune response against its own cells and tissues. (wikidoc.org)
  • This research will provide a better understanding of cellular and molecular mechanisms driving autoimmunity and help to develop therapeutic strategies targeting autoreactive T cells that escaped central tolerance. (news-medical.net)
  • Autoimmunity is the system of immune responses of an organism against its own healthy cells and tissues. (wikipedia.org)
  • Other T-cells can suppress or enhance autoimmunity (either in general or only for T lymphocytes in islets). (diabetesjournals.org)
  • Autoimmunity occurs when immune cells attack the other cells in the same organism. (qiagen.com)
  • We will focus on how dendritic cell subsets change the balance between major players in autoimmunity, namely Th1, Th17 and regulatory T cells. (ingentaconnect.com)
  • This process is not 100 percent reliable, and an unknown percent of potentially autoreactive T cells escape and may cause autoimmunity. (news-medical.net)
  • Significant changes in metabolite profiles (amino acids, lipids, fatty acids) precede islet autoimmunity in genetically at-risk children, which could be linked to inflammation and possibly apoptosis occurring in the pancreas [91,92], which has been linked to the PTPN2, a susceptibility gene expressed in islet cells that control apoptosis [93]. (diabetesincontrol.com)
  • Idiotypes and Autoimmunity (J. Kearney et al. (wiley.com)
  • The Human Inflammatory Response & Autoimmunity RT² Profiler PCR Array profiles the expression of 84 key genes involved in autoimmune and inflammatory immune responses. (qiagen.com)
  • Dilated Cardiomyopathy and The Role of Autoimmunity in. (bartleby.com)
  • We would also like to explore a third possibility-namely, the role of the lung in the aetiopathogenesis of autoimmunity. (bmj.com)
  • Rheumatoid arthritis is a type of arthritis in which autoimmunity causes the immune system to attack tissues in the joints, leading to muscle pain, joint deformities, fatigue, weakness, appetite loss, weight loss, and sometimes confinement to bed. (everydayhealth.com)
  • So all the immune reactions that we see in infection we also see in allergy, autoimmunity and conditions associated with inflammation. (drmyhill.co.uk)
  • Autoimmunity is all about allergy to our own body material, it is a completely useless reaction and, of course, destructive. (drmyhill.co.uk)
  • We found a one-third reduction in the incidence of islet autoimmunity, and this is high," she said. (medscape.com)
  • We also know from previous studies that the incidence of islet autoimmunity is higher in Finland and Sweden compared with the US. (medscape.com)
  • She also drew attention to the halving of incidence of islet autoimmunity with use of probiotics found in Sweden. (medscape.com)
  • Autoimmunity is now unequivocally regarded as the predominant pathogenic process underlying most forms of primary and secondary glomerulonephritis in humans. (bmj.com)